Arquivo da tag: Microbiologia

Bird flu is already a tragedy (The Atlantic)

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theatlantic.com

Katherine J. Wu

February 15, 2023

Eagles Are Falling, Bears Are Going Blind

Photo of a seabird, suspected to have died from H5N1, as seen through a worker's legs
Ernesto Benavides / AFP / Getty

It was late fall of 2022 when David Stallknecht heard that bodies were raining from the sky.

Stallknecht, a wildlife biologist at the University of Georgia, was already fearing the worst. For months, wood ducks had been washing up on shorelines; black vultures had been teetering out of tree tops. But now thousands of ghostly white snow-goose carcasses were strewn across agricultural fields in Louisiana, Missouri, and Arkansas. The birds had tried to take flight, only to plunge back to the ground. “People were saying they were literally dropping down dead,” Stallknecht told me. Even before he and his team began testing specimens in the lab, they suspected they knew what they would find: yet another crop of casualties from the deadly strain of avian influenza that had been tearing across North America for roughly a year.

Months later, the bird-flu outbreak continues to rage. An estimated 58.4 million domestic birds have died in the United States alone. Farms with known outbreaks have had to cull their chickens en masse, sending the cost of eggs soaring; zoos have herded their birds indoors to shield them from encounters with infected waterfowl. The virus has been steadily trickling into mammalian populations—foxes, bears, mink, whales, seals—on both land and sea, fueling fears that humans could be next. Scientists maintain that the risk of sustained spread among people is very low, but each additional detection of the virus in something warm-blooded and furry hints that the virus is improving its ability to infiltrate new hosts. “Every time that happens, it’s another chance for that virus to make the changes that it needs,” says Richard Webby, a virologist at St. Jude Children’s Research Hospital. “Right now, this virus is a kid in a candy store.”

A human epidemic, though, remains a gloomy forecast that may not come to pass. In the meantime, the outbreak has already been larger, faster-moving, and more devastating to North America’s wildlife than any other in recorded history, and has not yet shown signs of stopping. “I would use just one word to describe it: unprecedented,” says Shayan Sharif, an avian immunologist at Ontario Veterinary College. “We have never seen anything like this before.” This strain of bird flu is unlikely to be our next pandemic. But a flu pandemic has already begun for countless other creatures—and it could alter North America’s biodiversity for good.

Deadly strains of avian flu have been ferried onto North American shores multiple times before, and rapidly petered out. That was the case in 2014, when a highly virulent version of the virus crossed the Pacific from Asia and invaded U.S. poultry farms, forcing workers to exterminate millions of chickens and turkeys. The brutal interventions worked: “They did all the right things, and nipped it in the bud,” says Nicole Nemeth, a veterinary pathologist at the University of Georgia. Hardly any wild birds were affected; egg prices bumped up briefly, then settled back roughly to baseline. “It just kind of died down,” Nemeth told me. “And everyone breathed a sigh of relief.”

This time, though, the dynamics are different. The epidemic, which first erupted in Europe in the fall of 2021, appears to have crossed the Atlantic into Canada, then zigzagged down into the U.S. around the start of last year. American scientists have detected the virus in more than 150 wild and domestic avian species and at least a dozen different types of mammals. It’s by far the longest and most diverse list of victims the virus has ever claimed on this side of the world.

Some birds are likely to make it through the outbreak just fine. For as long as humans have been aware of this particular strain of avian influenza, scientifically classed as H5N1, the virus has been relatively gentle on certain types of waterfowl, especially mallards, pintails, and other so-called dabbling ducks. “Some populations have a prevalence as high as 40 percent, and they’re as normal as normal could be,” Stallknecht said. Those same species have also been some of avian flu’s best chauffeurs in the past, silently spreading the feces-borne infection across countries and continents during their seasonal migrations.

Others haven’t been so lucky. Some of the same respiratory issues that strike humans who have the flu—sneezing, coughing, pneumonia when the disease gets severe—can hit birds, too. But across a variety of susceptible species, necropsies show more extensive damage, with evidence of virus in various organs, including the liver, gut, and brain. The neurologic problems can be among the worst: Swans might swim in listless circles; geese might waddle shakily onto shores, their necks twisted and turned; eagles might flap defeatedly from their perches, unable to launch themselves into the air. Michelle Hawkins, a veterinarian at UC Davis, told me that several of the red-tailed hawks she’s treated in her clinic have arrived with their eyes shaking so vigorously from side to side that the spasms turn the animals’ head; others appear to gaze off into nothingness, unresponsive even when humans approach.

Death can come swiftly—sometimes within a day or two of the infection’s start. Birds simply keel over as if they’ve been shot, their bodies dropping like rocks. On poultry farms, outbreaks can wipe out entire flocks in just two or three days. In wilder settings, locals have spotted bald eagles plummeting out of their nests, leaving shrieking chicks behind. By the time infected birds reach Hawkins in her clinic, “they’re usually almost dead,” she told me. “And we can’t figure out how to help them except to put them out of their misery.” Hawkins estimated that in the past few months alone, her team’s euthanasia rate has gone up by about 50 percent.

Mammals so far haven’t fared much better. Last spring, the corpse of a dolphin infected with the virus was found wedged into a canal in Florida—around the same time that Wisconsin locals happened upon litters of ailing fox kits, drooling, twitching, and struggling to stand in the hours before they seized and died. In the fall, three young, flu-stricken grizzlies in Montana were euthanized after researchers noticed that the disoriented animals had begun to go blind. Wendy Puryear, a molecular virologist at Tufts University, told me that seals sick with the virus will sometimes convulse so badly that they can barely hold their bodies straight. Every seal she’s seen that tested positive has ended up dead within days. This month, researchers in Peru reported that they were picking up the virus in some of the sea lions that have died by the hundreds along the country’s coast; a similar situation may now be playing out among a number of Scotland’s seals.

It’s hard to say why this outbreak is so much worse than the ones that came before. Microbial evolution may be one culprit: Flu viruses are particularly inclined to tweak their RNA code; when two genetically distinct versions of the pathogens wind up in the same cell, they can also swap bits of their genomes. This iteration of H5N1 may be particularly adept at sparking lethal disease—something Justin Brown, a veterinary pathologist at Penn State, thinks is quite likely, given how many animals have died. It may also be more easily exiting birds’ bodies in feces, or more efficiently entering cells in the airway or gut. “This particular virus seems to be better adapted to wild birds. I think that’s the key thing,” Stallknecht told me. As climate change alters migration schedules, and pushes certain avian species into more frequent contact with one another’s contaminated scat, the risks of intermingling are only growing. The greater the number of infections, the more animals will die. “It becomes a numbers game,” Stallknecht said.

Flu viruses have never had much trouble spreading: They can be breathed out or defecated; they can persist on surfaces for hours, and in cool waters for days. But Webby suspects that the ballooning of this epidemic can be at least partly blamed on the severity of disease. “The easiest birds to catch are the ones that are sick,” he told me. Hawks, eagles, owls, and other predatory birds may be stumbling across dying ducks and eating them, unwittingly infecting themselves. Nemeth thinks that certain species, including black vultures, are now cutting out the middlebird and feasting on the carcasses of their own kin as they continue to die in droves. “They see dead tissue, they’re going to eat it,” she told me. It’s a morbid tragedy of abundance, as the virus climbs the food chain to reach species it hasn’t easily accessed before. “The biggest impact is on these atypical hosts,” Webby told me, which lack the prior exposures to the virus that might have helped protect them.

Predation or scavenging of sick or dead birds is probably how certain mammals—grizzlies, foxes, opossums, and the like—are catching the virus too. The seals and dolphins present a bit more of a puzzle, Puryear told me, though it’s possible to guess at what’s at play. At least some types of seals have been documented consuming birds; other marine mammals might simply be gulping feces-infested water. A recent avian-flu outbreak at a mink farm in Spain suggests a more troubling mode of transmission: mammals repeatedly conveying the virus to one another—a possible first for H5N1. “That is really disconcerting,” Sharif told me. “It tells me the virus is adapting to mammals.”

Animals vulnerable to the virus don’t have many good options for protection. Some avian-flu vaccines have been used on certain poultry farms, mostly abroad. But some of the same issues that plague human-flu vaccines are obstacles in the bird world too, Brown told me: The ingredients of the shots aren’t always good matches for the circulating virus, and the immunizations, which may be pretty good at staving off severe disease, don’t do much to block infection or transmission, making outbreaks tough to contain. Wild birds, which can’t be corralled and immunized en masse, are essentially out of luck. Nemeth told me that some of her colleagues in Florida have been trying to clear the ground of carcasses so that they won’t become sources of infection for yet another unlucky mammal or bird. “But they just can’t keep up with the number of deaths,” she said. Essentially all avian species are thought to be susceptible to infection—and there’s simply no way to reach every bird, says Becky Poulson, an avian-flu researcher at the University of Georgia. After hopscotching across the globe for decades, H5N1 now seems very likely to be in North America for good, “part of the new normal here,” Poulson told me.

Experts told me they’re hopeful that the outbreak will abate before long. But even if that happens, some species may not live to see it. North America’s birds already face a medley of threats—chemical pollution, window collisions, habitat destruction, roving colonies of feral cats—and some of them cannot sustain another blow. “This could be the last nail in the coffin for some species,” says Min Huang, who leads the migratory-bird program at Connecticut’s Department of Energy and Environmental Protection.

The current epidemic “may not be directly affecting us, in that almost none of us are getting sick,” says Kishana Taylor, a virologist at Rutgers University. But the extent of its reach into wildlife means that humans will still notice its many impacts. In a world with fewer birds, other animals—such as coyotes, snakes, and even humans—might go hungrier, while the fish, insects, and rats that birds eat could experience population booms. The treetops and shorelines, once alive with song, could go silent; far fewer seeds might be dispersed. The U.S.’s national bird—one of the country’s few conservation success stories—could once again find itself pushed to the brink. Some locals in the Southeast have already told Nemeth that they’re feeling the absence of vultures, as roadside deer carcasses begin to fester in the sun. The bird pandemic will have its survivors. But they are likely to be living in a world that is quieter, lonelier, and harsher than it was before.

Your Immune System Could Be Hurting You as a Way of Signalling to Others (Science Alert)

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sciencealert.com

Jonathan R Goodman, The Conversation – 13 May 2021

A major debate during the pandemic, and in infectious disease research more broadly, is why infected people die. No virus “wants” to kill anyone, as an epidemiologist once said to me. Like any other form of life, a virus’s goal is only to survive and reproduce.

A growing body of evidence instead suggests that the human immune system – which the science writer Ed Yong says is “where intuition goes to die” – may itself be responsible for many people’s deaths.

In an effort to find and kill the invading virus, the body can harm major organs, including the lungs and heart. This has led some doctors to focus on attenuating an infected patient’s immune response to help save them.

This brings up an evolutionary puzzle: what’s the point of the immune system if its overzealousness can kill the same people it evolved to defend?

The answer may lie in humanity’s evolutionary history: immunity may be as much about communication and behavior as it is about cellular biology. And to the degree that researchers can understand these broad origins of the immune system, they may be better positioned to improve responses to it.

The concept of the behavioral immune system is not new. Almost all humans sometimes feel disgust or revulsion – usually because whatever has made us feel that way poses a threat to our health.

And we aren’t alone in these reactions. Research shows that some animals avoid others that are showing symptoms of illness.

Eliciting care

However, more recent theoretical research suggests something more: humans, in particular, are likely to show compassion to those showing symptoms of illness or injury.

There’s a reason, this thinking goes, why people tend to exclaim when in pain, rather than just silently pull away from whatever is hurting them, and why fevers are linked to sluggish behavior.

Some psychologists argue that this is because immune responses are as much about communication as they are about self-maintenance. People who received care, over humanity’s history, probably tended to do better than those who tried to survive on their own.

In the broader evolutionary literature, researchers refer to these kinds of displays as “signals”. And like many of the innumerable signals we see across the natural world, immune-related signals can be used – or faked – to exploit the world around us, and each other.

Some birds, for example, feign injury to distract predators from their nests; rats suppress disease symptoms so that potential mates won’t ignore them.

We also see many illustrations of immune-signal use and misuse in human cultures. In The Adventure of the Dying Detective (1913), for example, Sherlock Holmes starves himself for three days to elicit a confession from a murder suspect. The suspect confesses only when he is convinced that his attempt to infect Holmes with a rare disease has been successful, misreading Holmes’s signs of illness.

This is an extreme example, but people feign signals of pain or illness all the time to avoid obligations, to elicit support from others, or even to avoid submitting an article by an agreed deadline. And this is an essential element of any signalling system.

Once a signal, be it a wince or a jaundiced complexion, elicits a response from whoever sees it, that response will start to drive how and why the signal is used.

Even germs use – and abuse – immune signals for their own gain. In fact, some viruses actually hijack our own immune responses, such as coughs and sneezes, to pass themselves on to new hosts, using our own evolved functions to further their interests.

Other germs, like SARS-CoV-2 (the virus that causes COVID-19) and Yersinia pestis (the bacterium that causes plague), can prevent our signalling to others when we are sick and pass themselves on without anyone realizing.

This perspective of immunity – one that takes into account biology, behavior and the social effects of illness – paints a starkly different picture from the more traditional view of the immune system as a collection of biological and chemical defenses against sickness.

Germs use different strategies, just as animals do, to exploit immune signals for their own purposes. And perhaps that’s what has made asymptomatically transmitted COVID-19 so damaging: people can’t rely on reading other people’s immune signals to protect themselves.

Insofar as doctors can predict how a particular infection – whether SARS-CoV-2, influenza, malaria or the next pathogen with pandemic potential – will interact with a patient’s immune system, they’ll be better positioned to tailor treatments for it. Future research will help us sort through the germs that hijack our immune signals – or suppress them – for their own purposes.

Viewing immunity not just as biological, but as a broader signalling system, may help us to understand our complex relationships with pathogens more effectively.

Jonathan R Goodman, PhD Candidate, Human Evolutionary Studies, University of Cambridge.

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Decision-making process of viruses could lead to new antibiotic treatments (Science Daily)

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Date:
February 6, 2017
Source:
Texas A&M AgriLife Communications
Summary:
Humans face hundreds of decisions every day. But we’re not alone. Even the tiniest viruses also make decisions, and scientists are researching how they do so, to help lead to better treatments for some diseases. A team of scientists has discovered how the lambda phage decides what actions to take in its host, the E. coli bacterium.

The lambda phage prefers to destroy E. coli bacteria, which makes it a prime target for researchers. Dr. Lanying Zeng, left, and her graduate student Jimmy Trinh developed a four-color fluorescence reporter system to track it at the single-virus level. Credit: Texas A&M AgriLife Research photo by Kathleen Phillips

Humans face hundreds of decisions every day. But we’re not alone. Even the tiniest viruses also make decisions, and scientists are researching how they do so, to help lead to better treatments for some diseases.

In a study published Feb. 6 in the journal Nature Communications, Dr. Lanying Zeng and her team at Texas A&M AgriLife Research discovered how the lambda phage decides what actions to take in its host, the E. coli bacterium.

A phage is a virus that infects and replicates within a bacterium. Phages were first discovered about 100 years ago, but recently scientists have begun to study how they can be used to attack disease-causing bacteria, especially strains that have become more resistant to antibiotics.

So numerous and diverse are phages — numbering into the billions, according to various reports in the U.S. National Library of Medicine — that researchers are now hot on the trail of phages that have the potential for curing specific bacterial maladies.

The lambda phage, for example, prefers to destroy E. coli bacteria, which makes it a prime target for researchers. In tracking that target, Zeng’s graduate student Jimmy Trinh developed a four-color fluorescence reporter system to track it at the single-virus level. This was combined with computational models devised by Dr. Gábor Balázsi, a biomedical engineer and collaborator at Stony Brook University in Stony Brook, New York, “to unravel both the interactions between phages and how individual phages determine” the fate of a cell.

What they found was not unlike the decision-making process of humans. Sometimes the lambda phage cooperates with others. Sometimes it competes.

“Instead of just the cell making a decision, we found the phage DNAs themselves also make decisions,” Zeng said.

Through the process they developed, the scientists were able to determine that timing played a role in decision-making.

Zeng explained that some phages can have two cycles of reproduction: lytic and lysogenic.

In the lytic cycle, full copies of the virus are made inside of a cell, say an E. coli cell. When the phage-infected cell becomes full of the replicating viruses, it bursts open and is destroyed. In the lysogenic cycle, the phage’s DNA lives as part of the bacterium itself and both continue to reproduce as one. In short, lysis involves competition while lysogeny involves cooperation, she said.

So, a key to using phages to destroy bacteria, Zeng said, is to understand how and when a phage decides to “go lytic” on the pathogen.

“Say you have two lambda phages that infect one cell,” she said. “Each phage DNA within the cell is capable of making a decision. We want to know how they make a decision, whether one is more dominant than the other, whether they have any interactions and compete to see who will win, or whether they compromise.”

“They may even coexist for some time and then finally choose one decision,” she said. “But the phage is making a subcellular decision — and that is very important. There could be a lot of implications.”

The four-color fluorescence reporter system helped the researchers visualize that many factors contribute to the decision and that “from the evolutionary point of view, the phages want to optimize their own fitness or survival,” she said. “So that is why they choose either lytic or lysogenic to maximize or optimize their survival.”

The team identified some of the factors that led to competition and others that led to cooperation.

Zeng said because phage therapy is a growing field for seeking ways to treat bacteria, the results of this study will help other scientists advance their research.

“This is a paradigm for bacteriophages,” she said. “When we understand the mechanism of the decision more, that can lead to more applications and better characterization of other systems.”

Journal Reference:

  1. Jimmy T. Trinh, Tamás Székely, Qiuyan Shao, Gábor Balázsi, Lanying Zeng. Cell fate decisions emerge as phages cooperate or compete inside their host. Nature Communications, 2017; 8: 14341 DOI: 10.1038/ncomms14341

How altered gut microbes cause obesity (Science Daily)

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Date:
June 8, 2016
Source:
Yale University
Summary:
Obesity is linked to changes in our gut microbes — the trillions of tiny organisms that inhabit our intestines. But the mechanism has not been clear to date. In a new study, a team of researchers has identified how an altered gut microbiota causes obesity.

Obesity is linked to changes in our gut microbes — the trillions of tiny organisms that inhabit our intestines. But the mechanism has not been clear. In a new study published in Nature, a Yale-led team of researchers has identified how an altered gut microbiota causes obesity.

In an earlier study, Gerald I. Shulman, M.D., the George R. Cowgill Professor of Medicine, observed that acetate, a short-chain fatty acid, stimulated the secretion of insulin in rodents. To learn more about acetate’s role, Shulman, who is also an investigator of the Howard Hughes Medical Institute, and a team of Yale researchers conducted a series of experiments in rodent models of obesity.

The research team compared acetate to other short-chain fatty acids and found higher levels of acetate in animals that consumed a high-fat diet. They also observed that infusions of acetate stimulated insulin secretion by beta cells in the pancreas, but it was unclear how.

Next, the researchers determined that when acetate was injected directly into the brain, it triggered increased insulin by activating the parasympathetic nervous system. “Acetate stimulates beta cells to secrete more insulin in response to glucose through a centrally mediated mechanism,” said Shulman. “It also stimulates secretion of the hormones gastrin and ghrelin, which lead to increased food intake.”

Finally, the research team sought to establish a causal relationship between the gut microbiota and increased insulin. After transferring fecal matter from one group of rodents to another, they observed similar changes in the gut microbiota, acetate levels, and insulin.

“Taken together these experiments demonstrate a causal link between alterations in the gut microbiota in response to changes in the diet and increased acetate production,” said Shulman. The increased acetate in turn leads to increased food intake, setting off a positive feedback loop that drives obesity and insulin resistance, he explained.

The study authors suggest that this positive feedback loop may have served an important role in evolution, by prompting animals to fatten up when they stumbled across calorically dense food in times of food scarcity.

“Alterations in the gut microbiota are associated with obesity and the metabolic syndrome in both humans and rodents,” Shulman noted. “In this study we provide a novel mechanism to explain this biological phenomenon in rodents, and we are now examining whether this mechanism translates to humans.”

Journal Reference:

  1. Rachel J. Perry, Liang Peng, Natasha A. Barry, Gary W. Cline, Dongyan Zhang, Rebecca L. Cardone, Kitt Falk Petersen, Richard G. Kibbey, Andrew L. Goodman, Gerald I. Shulman. Acetate mediates a microbiome–brain–β-cell axis to promote metabolic syndrome. Nature, 2016; 534 (7606): 213 DOI: 10.1038/nature18309

Teamwork enables bacterial survival (Science Daily)

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Strains of E. coli resistant to one antibiotic can protect other bacteria growing nearby

Date:
May 16, 2016
Source:
Massachusetts Institute of Technology
Summary:
Researchers have found that two strains of E. coli bacteria, each resistant to one antibiotic, can protect each other in an environment where both drugs are present.

Mutualism, a phenomenon in which different species benefit from their interactions with each other, can help bacteria form drug-resistant communities. Pictured is an artist’s interpretation of mutualism among bacteria. Credit: Jose-Luis Olivares/MIT

A new study from MIT finds that two strains of bacteria that are each resistant to one antibiotic can protect each other in an environment containing both drugs.

The findings demonstrate that mutualism, a phenomenon in which different species benefit from their interactions with each other, can help bacteria form drug-resistant communities. This is the first experimental demonstration in microbes of a type of mutualism known as cross-protection, which is more commonly seen in larger animals.

The researchers focused on two strains of E. coli, one resistant to ampicillin and the other resistant to chloramphenicol. These bacteria and many others defend themselves from antibiotics by producing enzymes that break down the antibiotics. As a side effect, this also protects cells that don’t produce those enzymes, by removing the antibiotic from the environment.

“Any time that you’re breaking down an antibiotic, there’s this potential for cross-protection,” says Jeff Gore, the Latham Family Career Development Associate Professor of Physics and the senior author of the study, which appears in the Proceedings of the National Academy of Sciences the week of May 16.

The MIT team found that, indeed, both strains could survive in an environment where both antibiotics were present, even though each was only resistant to one of the drugs. This type of situation is likely also found in the natural world, especially in soil where many strains of bacteria live together.

“Each of them is making different toxins and each of them is resistant to different toxins,” Gore says. “A lot of antibiotics are produced by microbes as part of the combat that is taking place between microorganisms in the soil.”

Gore and co-first authors Eugene Yurtsev and Arolyn Conwill, both MIT graduate students, also found that the populations of the two strains oscillate over time. Population oscillations are common in predator-prey interactions but rare in mutualistic interactions such as the cross-protection seen in this study.

Throughout their experiments, the researchers diluted the bacterial population each day by transferring about 1 percent of the population to a new test tube, to which new antibiotics were added. They found that while the total size of the bacterial population remained about the same, there were large oscillations in the relative percentages of each strain, which varied by nearly 1,000 percent over a period of about three days.

For example, if the ampicillin-resistant strain was more abundant in the beginning of a cycle, it rapidly deactivated ampicillin in the environment, allowing the chloramphenicol-resistant strain to begin growing. The ampicillin-resistant strain only began growing once the other strain had expanded enough to deactivate most of the chloramphenicol, at which point the chloramphenicol-resistant strain had already overtaken the ampicillin-resistant strain.

“The mutualism exhibits oscillations because the strain that is more abundant at the beginning of a growth cycle might end up less abundant at the end of that cycle,” Gore says.

At lower antibiotic concentrations, the bacterial population can survive in this oscillating pattern indefinitely, but at higher drug concentrations, the oscillations destabilize the population, and it eventually collapses.

Gore suspects that similar population oscillations may also be seen in natural environments such as the human gut, as bacteria exit the body along with bowel movements, or in soil as bacteria are washed away by rainfall.

Gore’s lab is now looking at this type of mutualism in bacteria living in the gut of the worm C. elegans. The researchers are also studying how these types of population oscillations can become synchronized over large geographic areas, and how migration between populations influences this synchronization.

Journal Reference:

  1. Saurabh R. Gandhi, Eugene Anatoly Yurtsev, Kirill S. Korolev, and Jeff Gore. Range expansions transition from pulled to pushed waves as growth becomes more cooperative in an experimental microbial population. PNAS, 2016 DOI: 10.1073/pnas.1521056113

A single-celled organism capable of learning (Science Daily)

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Date:
April 27, 2016
Source:
CNRS
Summary:
For the first time, scientists have demonstrated that an organism devoid of a nervous system is capable of learning. Biologists have succeeded in showing that a single-celled organism, the protist, is capable of a type of learning called habituation. This discovery throws light on the origins of learning ability during evolution, even before the appearance of a nervous system and brain. It may also raise questions as to the learning capacities of other extremely simple organisms such as viruses and bacteria.

The slime mold Physarum polycephalum (diameter: around 10 centimeters), made up of a single cell, was here cultivated in the laboratory on agar gel. Credit: Audrey Dussutour (CNRS)

For the first time, scientists have demonstrated that an organism devoid of a nervous system is capable of learning. A team from the Centre de Recherches sur la Cognition Animale (CNRS/Université Toulouse III — Paul Sabatier) has succeeded in showing that a single-celled organism, the protist Physarum polycephalum, is capable of a type of learning called habituation. This discovery throws light on the origins of learning ability during evolution, even before the appearance of a nervous system and brain. It may also raise questions as to the learning capacities of other extremely simple organisms such as viruses and bacteria. These findings are published in the Proceedings of the Royal Society B on 27 April 2016.

An ability to learn, and memory are key elements in the animal world. Learning from experiences and adapting behavior accordingly are vital for an animal living in a fluctuating and potentially dangerous environment. This faculty is generally considered to be the prerogative of organisms endowed with a brain and nervous system. However, single-celled organisms also need to adapt to change. Do they display an ability to learn? Bacteria certainly show adaptability, but it takes several generations to develop and is more a result of evolution. A team of biologists thus sought to find proof that a single-celled organism could learn. They chose to study the protist, or slime mold, Physarum polycephalum, a giant cell that inhabits shady, cool areas[1] and has proved to be endowed with some astonishing abilities, such as solving a maze, avoiding traps or optimizing its nutrition[2]. But until now very little was known about its ability to learn.

During a nine-day experiment, the scientists thus challenged different groups of this mold with bitter but harmless substances that they needed to pass through in order to reach a food source. Two groups were confronted either by a “bridge” impregnated with quinine, or with caffeine, while the control group only needed to cross a non-impregnated bridge. Initially reluctant to travel through the bitter substances, the molds gradually realized that they were harmless, and crossed them increasingly rapidly — behaving after six days in the same way as the control group. The cell thus learned not to fear a harmless substance after being confronted with it on several occasions, a phenomenon that the scientists refer to as habituation. After two days without contact with the bitter substance, the mold returned to its initial behavior of distrust. Furthermore, a protist habituated to caffeine displayed distrustful behavior towards quinine, and vice versa. Habituation was therefore clearly specific to a given substance.

Habituation is a form of rudimentary learning, which has been characterized in Aplysia (an invertebrate also called sea hare)[3]. This form of learning exists in all animals, but had never previously been observed in a non-neural organism. This discovery in a slime mold, a distant cousin of plants, fungi and animals that appeared on Earth some 500 million years before humans, improves existing understanding of the origins of learning, which markedly preceded those of nervous systems. It also offers an opportunity to study learning types in other very simple organisms, such as viruses or bacteria.

[1] This single cell, which contains thousands of nuclei, can cover an area of around a square meter and moves within its environment at speeds that can reach 5 cm per hour.

[2] See “Even single-celled organisms feed themselves in a ‘smart’ manner.” https://www.sciencedaily.com/releases/2010/02/100210164712.htm

[3] Mild tactile stimulation of the animal’s siphon normally causes the defensive reflex of withdrawing the branchiae. If the harmless tactile stimulation is repeated, this reflex diminishes and finally disappears, thus indicating habituation.

Journal Reference:

  1. Romain P. Boisseau, David Vogel, Audrey Dussutour. Habituation in non-neural organisms: evidence from slime moulds. Proceedings of the Royal Society B: Biological Sciences, 2016; 283 (1829): 20160446 DOI: 10.1098/rspb.2016.0446

New appreciation for human micro biome leads to greater understanding of human health (Science Daily)

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Date: February 14, 2016

Source: University of Oklahoma

Summary: Anthropologists are studying the ancient and modern human micro biome and the role it plays in human health and disease. By applying genomic and proteomic sequencing technologies to ancient human microbiomes, such as coprolites and dental calculus, as well as to contemporary microbiomes in traditional and industrialized societies, Researchers are advancing the understanding of the evolutionary history of our microbial self and its impact on human health today.

University of Oklahoma anthropologists are studying the ancient and modern human microbiome and the role it plays in human health and disease. By applying genomic and proteomic sequencing technologies to ancient human microbiomes, such as coprolites and dental calculus, as well as to contemporary microbiomes in traditional and industrialized societies, OU researchers are advancing the understanding of the evolutionary history of our microbial self and its impact on human health today.

Christina Warinner, professor in the Department of Anthropology, OU College of Arts and Sciences, will present, “The Evolution and Ecology of Our Microbial Self,” during the American Association for the Advancement of Science panel on Evolutionary Biology Impacts on Medicine and Public Health, at 1:30 pm, Sunday, Feb. 14, 2016 in the Marriott Marshall Ballroom West, Washington, DC. Warinner will discuss how major events, such as the invention of agriculture and the advent of industrialization, have affected the human microbiome.

“We don’t have a complete picture of the microbiome,” Warinner said. “OU research indicates human behavior over the past 2000 years has impacted the gut microbiome. Microbial communities have become disturbed, but before we can improve our health, we have to understand our ancestral microbiome. We cannot make targeted or informed interventions until we know that. Ancient samples allow us to directly measure changes in the human microbiome at specific times and places in the past.”

Warinner and colleague, Cecil M. Lewis, Jr., co-direct OU’s Laboratories of Molecular Anthropology and Microbiome Research and the research focused on reconstructing the ancestral human oral and gut microbiome, addressing questions concerning how the relationship between humans and microbes has changed through time and how our microbiomes influence health and disease in diverse populations, both today and in the past. Warinner and Lewis are leaders in the field of paleogenomics, and the OU laboratories house the largest ancient DNA laboratory in the United States.

Warinner is pioneering the study of ancient human microbiomes, and in 2014 she published the first detailed metagenomics and metaproteomic characterization of the ancient oral microbiome in the journal Nature Genetics. In 2015, she published a study on the identification of milk proteins in ancient dental calculus and the reconstruction of prehistoric European dairying practices. In the same year, she was part of an international team that published the first South American hunter-gatherer gut microbiome and identified Treponema as a key missing ancestral microbe in industrialized societies.

Ancient viral molecules essential for human development (Science Daily)

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Date: November 23, 2015

Source: Stanford University Medical Center

Summary: Genetic material from ancient viral infections is critical to human development, according to researchers.

Rendering of a virus among blood cells. Credit: © ysfylmz / Fotolia

Genetic material from ancient viral infections is critical to human development, according to researchers at the Stanford University School of Medicine.

They’ve identified several noncoding RNA molecules of viral origins that are necessary for a fertilized human egg to acquire the ability in early development to become all the cells and tissues of the body. Blocking the production of this RNA molecule stops development in its tracks, they found.

The discovery comes on the heels of a Stanford study earlier this year showing that early human embryos are packed full of what appear to be viral particles arising from similar left-behind genetic material.

“We’re starting to accumulate evidence that these viral sequences, which originally may have threatened the survival of our species, were co-opted by our genomes for their own benefit,” said Vittorio Sebastiano, PhD, an assistant professor of obstetrics and gynecology. “In this manner, they may even have contributed species-specific characteristics and fundamental cell processes, even in humans.”

Sebastiano is a co-lead and co-senior author of the study, which will be published online Nov. 23 in Nature Genetics. Postdoctoral scholar Jens Durruthy-Durruthy, PhD, is the other lead author. The other senior author of the paper is Renee Reijo Pera, PhD, a former professor of obstetrics and gynecology at Stanford who is now on the faculty of Montana State University.

Sebastiano and his colleagues were interested in learning how cells become pluripotent, or able to become any tissue in the body. A human egg becomes pluripotent after fertilization, for example. And scientists have learned how to induce other, fully developed human cells to become pluripotent by exposing them to proteins known to be present in the very early human embryo. But the nitty-gritty molecular details of this transformative process are not well understood in either case.

An ancient infection

The researchers knew that a type of RNA molecules called long-intergenic noncoding, or lincRNAs, have been implicated in many important biological processes, including the acquisition of pluripotency. These molecules are made from DNA in the genome, but they don’t go on to make proteins. Instead they function as RNA molecules to affect the expression of other genes.

Sebastiano and Durruthy-Durruthy used recently developed RNA sequencing techniques to examine which lincRNAs are highly expressed in human embryonic stem cells. Previously, this type of analysis was stymied by the fact that many of the molecules contain highly similar, very repetitive regions that are difficult to sequence accurately.

They identified more than 2,000 previously unknown RNA sequences, and found that 146 are specifically expressed in embryonic stem cells. They homed in on the 23 most highly expressed sequences, which they termed HPAT1-23, for further study. Thirteen of these, they found, were made up almost entirely of genetic material left behind after an eons-ago infection by a virus called HERV-H.

HERV-H is what’s known as a retrovirus. These viruses spread by inserting their genetic material into the genome of an infected cell. In this way, the virus can use the cell’s protein-making machinery to generate viral proteins for assembly into a new viral particle. That particle then goes on to infect other cells. If the infected cell is a sperm or an egg, the retroviral sequence can also be passed to future generations.

HIV is one common retrovirus that currently causes disease in humans. But our genomes are also littered with sequences left behind from long-ago retroviral infections. Unlike HIV, which can go on to infect new cells, these retroviral sequences are thought to be relatively inert; millions of years of evolution and accumulated mutations mean that few maintain the capacity to give instructions for functional proteins.

After identifying HPAT1-23 in embryonic stem cells, Sebastiano and his colleagues studied their expression in human blastocysts — the hollow clump of cells that arises from the egg in the first days after fertilization. They found that HPAT2, HPAT3 and HPAT5 were expressed only in the inner cell mass of the blastocyst, which becomes the developing fetus. Blocking their expression in one cell of a two-celled embryo stopped the affected cell from contributing to the embryo’s inner cell mass. Further studies showed that the expression of the three genes is also required for efficient reprogramming of adult cells into induced pluripotent stem cells.

Sequences found only in primates

“This is the first time that these virally derived RNA molecules have been shown to be directly involved with and necessary for vital steps of human development,” Sebastiano said. “What’s really interesting is that these sequences are found only in primates, raising the possibility that their function may have contributed to unique characteristics that distinguish humans from other animals.”

The researchers are continuing their studies of all the HPAT molecules. They’ve learned that HPAT-5 specifically affects pluripotency by interacting with and sequestering members of another family of RNAs involved in pluripotency called let-7.

“Previously retroviral elements were considered to be a class that all functioned in basically the same way,” said Durruthy-Durruthy. “Now we’re learning that they function as individual elements with very specific and important roles in our cells. It’s fascinating to imagine how, during the course of evolution, primates began to recycle these viral leftovers into something that’s beneficial and necessary to our development.”

Journal Reference:

  1. Jens Durruthy-Durruthy, Vittorio Sebastiano, Mark Wossidlo, Diana Cepeda, Jun Cui, Edward J Grow, Jonathan Davila, Moritz Mall, Wing H Wong, Joanna Wysocka, Kin Fai Au, Renee A Reijo Pera. The primate-specific noncoding RNA HPAT5 regulates pluripotency during human preimplantation development and nuclear reprogramming. Nature Genetics, 2015; DOI: 10.1038/ng.3449

Gut microbes signal to the brain when they’re full (Science Daily)

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Date: November 24, 2015

Source: Cell Press

Summary: Don’t have room for dessert? The bacteria in your gut may be telling you something. Twenty minutes after a meal, gut microbes produce proteins that can suppress food intake in animals, reports a study. The researchers also show how these proteins injected into mice and rats act on the brain reducing appetite, suggesting that gut bacteria may help control when and how much we eat.

These are neurons (c-fos, green) in the rat central amygdala activated by E. coli proteins in stationary phase and surrounded by nerve terminals (calcitonin gene-related peptide, red) originating from anorexigenic brainstem projections. Credit: J. Breton, N. Lucas & D. Schapman.

Don’t have room for dessert? The bacteria in your gut may be telling you something. Twenty minutes after a meal, gut microbes produce proteins that can suppress food intake in animals, reports a study published November 24 in Cell Metabolism. The researchers also show how these proteins injected into mice and rats act on the brain reducing appetite, suggesting that gut bacteria may help control when and how much we eat.

The new evidence coexists with current models of appetite control, which involve hormones from the gut signalling to brain circuits when we’re hungry or done eating. The bacterial proteins–produced by mutualistic E. coli after they’ve been satiated–were found for the first time to influence the release of gut-brain signals (e.g., GLP-1 and PYY) as well as activate appetite-regulated neurons in the brain.

“There are so many studies now that look at microbiota composition in different pathological conditions but they do not explore the mechanisms behind these associations,” says senior study author Sergueï Fetissov of Rouen University and INSERM’s Nutrition, Gut & Brain Laboratory in France. “Our study shows that bacterial proteins from E. coli can be involved in the same molecular pathways that are used by the body to signal satiety, and now we need to know how an altered gut microbiome can affect this physiology.”

Mealtime brings an influx of nutrients to the bacteria in your gut. In response, they divide and replace any members lost in the development of stool. The study raises an interesting theory: since gut microbes depend on us for a place to live, it is to their advantage for populations to remain stable. It would make sense, then, if they had a way to communicate to the host when they’re not full, promoting host to ingest nutrients again.

In the laboratory, Fetissov and colleagues found that after 20 minutes of consuming nutrients and expanding numbers, E. coli bacteria from the gut produce different kinds of proteins than they did before their feeding. The 20 minute mark seemed to coincide with the amount of time it takes for a person to begin feeling full or tired after a meal. Excited over this discovery, the researcher began to profile the bacterial proteins pre- and post-feeding.

They saw that injection of small doses of the bacterial proteins produced after feeding reduced food intake in both hungry and free-fed rats and mice. Further analysis revealed that “full” bacterial proteins stimulated the release of peptide YY, a hormone associated with satiety, while “hungry” bacterial hormones did not. The opposite was true for glucagon-like peptide-1 (GLP-1), a hormone known to simulate insulin release.

The investigators next developed an assay that could detect the presence of one of the “full” bacterial proteins, called ClpB in animal blood. Although blood levels of the protein in mice and rats detected 20 minutes after meal consumption did not change, it correlated with ClpB DNA production in the gut, suggesting that it may link gut bacterial composition with the host control of appetite. The researchers also found that ClpB increased firing of neurons that reduce appetite. The role of other E.coli proteins in hunger and satiation, as well as how proteins from other species of bacteria may contribute, is still unknown.

“We now think bacteria physiologically participate in appetite regulation immediately after nutrient provision by multiplying and stimulating the release of satiety hormones from the gut,” Fetisov says. “In addition, we believe gut microbiota produce proteins that can be present in the blood longer term and modulate pathways in the brain.”

Journal Reference:

  1. Jonathan Breton, Naouel Tennoune, Nicolas Lucas, Marie Francois, Romain Legrand, Justine Jacquemot, Alexis Goichon, Charlène Guérin, Johann Peltier, Martine Pestel-Caron, Philippe Chan, David Vaudry, Jean-Claude do Rego, Fabienne Liénard, Luc Pénicaud, Xavier Fioramonti, Ivor S. Ebenezer, Tomas Hökfelt, Pierre Déchelotte, Sergueï O. Fetissov. Gut Commensal E. coli Proteins Activate Host Satiety Pathways following Nutrient-Induced Bacterial Growth. Cell Metabolism, 2015; DOI: 10.1016/j.cmet.2015.10.017

Scientists call for national effort to understand and harness Earth’s microbes (Science Daily)

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Berkeley Lab researchers co-author Science article proposing Unified Microbiome Initiative

Date:
October 29, 2015
Source:
DOE/Lawrence Berkeley National Laboratory
Summary:
To understand and harness the capabilities of Earth’s microbial ecosystems, nearly fifty scientists propose a national effort in the US called the Unified Microbiome Initiative.

This colorized microscopy image hints at the complexity of microbial life. It shows two bacterial cells in soil. The bacteria glue clay particles together and protect themselves from predators. This also stabilizes soil and stores carbon that could otherwise enter the atmosphere. Credit: Manfred Auer, Berkeley Lab

Microbes are essential to life on Earth. They’re found in soil and water and inside the human gut. In fact, nearly every habitat and organism hosts a community of microbes, called a microbiome. What’s more, microbes hold tremendous promise for innovations in medicine, energy, agriculture, and understanding climate change.

Scientists have made great strides learning the functions of many microbes and microbiomes, but this research also highlights how much more there is to know about the connections between Earth’s microorganisms and a vast number of processes. Deciphering how microbes interact with each other, their hosts, and their environment could transform our understanding of the planet. It could also lead to new antibiotics, ways to fight obesity, drought-resistant crops, or next-gen biofuels, to name a few possibilities.

To understand and harness the capabilities of Earth’s microbial ecosystems, nearly fifty scientists from Department of Energy national laboratories, universities, and research institutions have proposed a national effort called the Unified Microbiome Initiative. The scientists call for the initiative in a policy forum entitled “A unified initiative to harness Earth’s microbiomes” published Oct. 30, 2015, in the journal Science.

The Unified Microbiome Initiative would involve many disciplines, including engineering, physical, life, and biomedical sciences; and collaborations between government institutions, private foundations, and industry. It would also entail the development of new tools that enable a mechanistic and predictive understanding of Earth’s microbial processes.

Among the authors of the Science article are several scientists from the Department of Energy’s Lawrence Berkeley National Laboratory (Berkeley Lab). These are Berkeley Lab Director Paul Alivisatos; Eoin Brodie, Deputy Director of the Climate and Ecosystem Sciences Division; Mary Maxon, the Biosciences Area Principal Deputy; Eddy Rubin, Director of the Joint Genome Institute; and Peidong Yang, a Faculty Scientist in the Materials Sciences Division. Alivisatos is also the Director of the Kavli Energy Nanoscience Institute, and Yang is the Co-Director.

Berkeley Lab has a long history of microbial research, from its pioneering work in metagenomics at the Joint Genome Institute, to the more recent Microbes to Biomes initiative, which is designed to harness microbes in ways that protect fuel and food supplies, environmental security, and health.

The call for the Unified Microbiome Initiative comes at a critical time in microbial research. DNA sequencing has enabled scientists to detect microbes in every biological system, thriving deep underground and inside insects for example, and in mind-boggling numbers: Earth’s microbes outnumber the stars in the universe. But to benefit from this knowledge, this descriptive phase must transition to a new phase that explores how microbial communities function, how to predict their actions, and how to make use of them.

“Technology has gotten us to the point where we realize that microbes are like dark matter in the universe. We know microbes are everywhere, and are far more complex than we previously thought, but we really need to understand how they communicate and relate to the environment,” says Brodie.

“And just like physicists are trying to understand dark matter, we need to understand the functions of microbes and their genes. We need to study what life is like at the scale of microbes, and how they relate to the planet,” Brodie adds.

This next phase of microbiome research will require strong ties between disciplines and institutions, and new technologies that accelerate discovery. The scientists map out several opportunities in the Science article. These include:

  • Tools to understand the biochemical functions of gene products, a large portion of which are unknown.
  • Technologies that quickly generate complete genomes from individual cells found in complex microbiomes.
  • Imaging capabilities that visualize individual microbes, along with their interactions and chemical products, in complex microbial networks.
  • Adaptive models that capture the complexity of interactions from molecules to microbes, and from microbial communities to ecosystems.

Many of these new technologies would be flexible platforms, designed initially for microbial research, but likely to find uses in other fields.

Ten years after the launch of the Unified Microbiome Initiative, the authors of the Science article envision an era in which a predictive understanding of microbial processes enables scientists to manage and design microbiomes in a responsible way–a key step toward harnessing their capabilities for beneficial applications.

“This is an incredibly exciting time to be involved in microbial research,” says Brodie. “It has the potential to contribute to so many advances, such as in medicine, energy, agriculture, biomanufacturing, and the environment.”

Journal Reference:

  1. A. P. Alivisatos, M. J. Blaser, E. L. Brodie, M. Chun, J. L. Dangl, T. J. Donohue, P. C. Dorrestein, J. A. Gilbert, J. L. Green, J. K. Jansson, R. Knight, M. E. Maxon, M. J. McFall-Ngai, J. F. Miller, K. S. Pollard, E. G. Ruby, S. A. Taha. A unified initiative to harness Earth’s microbiomes. Science, 2015; 350 (6260): 507 DOI: 10.1126/science.aac8480

Brasileiro faz música em dueto com fungo (BBC)

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Roland Pease – Da BBC Radio Science

10 março 2015

Crédito: Edurado Miranda e Ed Braun

Biocomputador com mofo toca dueto com piano

Um músico brasileiro apresentou na Grã-Bretanha um dueto inédito: no piano, ele interagiu com um fungo.

E mofo toca música? Nas mãos de Eduardo Miranda, sim.

Especialista em música computadorizada, ele transformou a decomposição em composição: seu novo trabalho usa culturas do fungo Physarum polycephalumcomo um componente central de um biocomputador interativo, que recebe sinais de som e envia de volta as respostas.

“A composição, Biocomputer Music, se desenvolve como uma interação entre mim e a máquina Physarum,” disse Miranda.

“Eu toco alguma coisa, o sistema escuta, toca alguma coisa de volta, e então eu respondo, e assim por diante.”

Brasileiro de Porto Alegre, Miranda leciona na Universidade de Plymouth, na Inglaterra.

Ele disse à BBC Brasil que Heitor Villa-Lobos tem uma grande inflluência em sua obra e que gostaria de levar a apresentação Biocomputer para o Brasil, mas que, por enquanto, questões técnicas impedem que ele viaje com o equipamento.

Funcionamento

O mofo Physarum forma um componente eletrônico vivo e mutante em um circuito que processa sons captados por um microfone treinado no piano.

Credito: Eduardo Miranda e Ed Braun

Projeto foi desenvolvido na Universidade de Plymouth

Pequenos tubos formados pelo Physarum têm a propriedade elétrica de agir como uma resistência variável que muda de acordo com tensões aplicadas anteriormente, de acordo com Ed Braund, aluno de doutorado no Centro Interdisciplinar de Computer Music Research na Universidade de Plymouth.

“As notas de piano são transformados em uma onda elétrica complexa que enviamos através de um desses túbulos Physarum. A resistência Physarum muda em função das entradas anteriores, e as notas musicais viram, então, uma nova saída que é então enviada de volta para o piano. O biocomputador atua como um dispositivo de memória”, acrescenta Miranda.

“Quando você diz a ele para tocar novamente, ele vai embaralhar as notas enviadas. Pode até gerar alguns sons que não estavam nas notas tocadas. A máquina tem um pouco de ‘criatividade’.”

Enquanto o pianista toca piano na forma convencional, utilizando as teclas, o biocomputador induz notas por pequenos eletroímãs que pairam milímetros acima das cordas de metal, imbuindo a música com um tom etéreo.

Acaso

Miranda compara seu uso de um biocomputador às técnicas “aleatórias” do compositor de vanguarda americano John Cage (1912-1992), que se voltou para o livro chinês de mudanças i-ching e ao lançamento de dados para controlar partes de suas composições.

Credito: Eduardo Miranda e Ed Braund

Som de computador tem traço ‘etéreo’

“John Cage acreditava no acaso, mas não na aleatoriedade. Ele queria aproveitar a estrutura que estava fora de seu controle. Aqui nós temos o efeito, programado em uma máquina viva. Eu acho que isso é o sonho de John Cage realizado.”

Miranda vem explorando há algum tempo o uso de computadores em peças interativas de composições eletrônicas, mas valoriza a simplicidade do processador Physarum.

“O que eu ouço é muito diferente de ter um computador digital programado com cadeias de dados. Não é inteligente, mas é vivo. O que é interessante…”

A estreia de Biocomputer Music ocorreu no Peninsular Arts Contemporary Music Festival “Biomusic” no dia 1º de março.

Você sabia que a maior parte das células do seu corpo não é humana? (UOL)

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Tatiana Pronin

Do UOL, em São Paulo

20/01/201506h00

Micróbios infestam nosso corpo: mas sem eles, ninguém é tão humano

Micróbios infestam nosso corpo: mas sem eles, ninguém é tão humano

É de deixar qualquer um espantado: 90% das células presentes no nosso corpo não são humanas. Em outras palavras, você é muito mais micróbios do que você mesmo. Esses “invasores”, embora “invisíveis”, são fundamentais para o nosso equilíbrio. Mas qualquer deslize nesse ecossistema pode causar doenças, muitas delas graves. Por isso, não se descuide: o perigo mora dentro de você e também fora, na superfície da sua pele.

Especialista no tema, o pesquisador Luis Caetano Antunes, da Escola Nacional de Saúde Pública Sergio Arouca, da Fundação Oswaldo Cruz, explica que os seres humanos são colonizados por mais de 35 mil espécies diferentes de bactérias, segundo algumas estimativas. “Lembrando que esse número não leva em conta vírus, protozoários etc”, esclarece.

Considerando apenas um indivíduo, a estimativa é de mais de mil espécies diferentes. “Já se você considerar cepas (que são indivíduos pertencentes à mesma espécie, mas com características peculiares), esse número sobe para mais de 7 mil”, diz. Se você pudesse colocar todas elas numa balança, os ponteiros marcariam aproximadamente 1 kg.

Essa microbiota (flora e fauna microscópica de uma região) é formada assim que chegamos ao mundo. Antunes afirma, inclusive, que bebês nascidos por parto normal têm micróbios diferentes daqueles que nascem por cesariana, pois o contato com o canal vaginal da mãe funciona como um “primeiro banho” de micro-organismos.

Intestino é albergue

Apesar de se estabilizar depois que a pessoa completa 1 ano de idade, a população de micro-organismos está sempre em evolução, graças ao contato com o ambiente externo. Assim, a variedade e a quantidade são maiores em locais mais expostos, como boca, pele, olhos, estômago, intestino, tratos respiratórios, genitais e urinários.

A parte do nosso corpo mais colonizada é de longe o intestino, com 70% do total de bactérias, segundo o pesquisador. “Um dos motivos é que o intestino possui uma quantidade grande de nutrientes para as bactérias. Além disso, ainda existem secreções, células humanas mortas etc”, diz Luis Caetano Antunes.

O especialista também chama atenção para o tamanho desse órgão, que é cheio de vilosidades (dobras, basicamente). “O intestino humano, quando esticado, tem área equivalente a uma quadra de tênis, ou cerca de 200 metros quadrados”, informa.

Médicos, cientistas e nutricionistas têm alertado para a importância da microbiota intestinal. Não é à toa que produtos com lactobacilos se tornaram mais comuns nas prateleiras dos supermercados.

Antunes descreve três funções principais desse exército de micróbios. A primeira é a nutrição: “Os micro-organismos intestinais auxiliam na degradação de nutrientes que o ser humano, sozinho, não conseguiria degradar”, diz. Além disso, eles produzem substâncias, como vitaminas, que nós não produzimos, e afetam as células para que elas consigam extrair mais energia da dieta.

A segunda é treinar o sistema imunológico, fazendo-o identificar o que representa ou não uma ameaça ao nosso organismo. “Um exemplo dessa função vem da observação de que hoje em dia as taxas de doenças relacionadas ao sistema imune (doenças alérgicas, principalmente) está muito mais alta, e isso tem sido associado ao uso indiscriminado de antibióticos, aumento no número de partos por cesariana e excesso de limpeza”, comenta o pesquisador.

A terceira (e não menos importante) missão da microbiota é nos defender contra agentes nocivos. “Sem as bactérias naturais do nosso corpo ficamos muito mais vulneráveis aos ataques de bactérias perigosas”, garante Luis Caetano Antunes, lembrando que há uma série de infecções que são mais comuns em pessoas com histórico de uso recente de antibióticos. “Eles matam as bactérias inofensivas, abrindo espaço para que outras bactérias invadam o nosso organismo e causem doenças.”

Boca cheia

Um dos primeiros cientistas a observar a existência de comunidades de bactérias em nosso corpo foi o holandês Antonie van Leeuwenhoek, que no século 17 analisou um raspado da superfície de seus dentes e descobriu um grande número de seres vivos minúsculos.

Uma organização também holandesa, chamada TNO, divulgou recentemente, após um estudo, que nossa boca abriga cerca de 700 variedades diferentes de bactérias. Os pesquisadores descobriram que um único beijo de língua é capaz de transferir 80 milhões de bactérias de uma boca para outra. Os dados foram publicados na revista Microbiome.

Algumas pessoas podem ficar enojadas, mas a verdade é que beijar pode ser uma maneira de fortalecer o sistema imunológico, tomando por base a lógica descrita pelo pesquisador da Fiocruz.

Pele que habito

Se os micróbios do intestino representam um exército estratégico dentro do corpo, os que habitam nossa pele são a linha de frente. “É a armadura que nos protege contra agentes externos”, considera o médico Jayme de Oliveira Filho, vice-presidente da Sociedade Brasileira de Dermatologia.

Assim como na selva a falta de leões pode levar ao excesso de zebras, qualquer desequilíbrio na microbiota da pele pode levar a problemas variados. A integridade pode ser afetada por banhos longos e quentes, e até pelo uso excessivo de álcool em gel e sabonetes antibacterianos. “Se você usa um produto que promete matar 99% das bactérias, ainda sobrarão muitas, mas você pode matar aquelas que são úteis à pele”, diz o médico.

Tomar muito sol sem filtro também é uma forma de agredir a cútis. É por isso que muita gente tem crises de herpes labial, doença provocada por vírus, depois que volta da praia. Ou adquire manchas nos braços e nas costas (pitiríase versicolor), provocadas por um tipo de fungo. O médico avisa que algumas famílias são mais predispostas a certos tipos de micro-organismos. Se a integridade da pele é afetada, você pode desenvolver um problema que nunca havia aparecido antes. E, acredite, pode até pegar gripe com mais facilidade.

Bacterial ‘communication system’ could be used to stop, kill cancer cells, study finds (Science Daily)

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Date: September 24, 2014

Source: University of Missouri-Columbia

Summary: A molecule used as a communication system by bacteria can be manipulated to prevent cancer cells from spreading, a study has demonstrated. “During an infection, bacteria release molecules which allow them to ‘talk’ to each other,” said the lead author of the study. “Depending on the type of molecule released, the signal will tell other bacteria to multiply, escape the immune system or even stop spreading.”

Bacteria molecule kills cancer cells: Cancer cells on the left are pre-molecule treatment. The cells on the right are after the treatment and are dead. Credit: Image courtesy of University of Missouri-Columbia

Cancer, while always dangerous, truly becomes life-threatening when cancer cells begin to spread to different areas throughout the body. Now, researchers at the University of Missouri have discovered that a molecule used as a communication system by bacteria can be manipulated to prevent cancer cells from spreading. Senthil Kumar, an assistant research professor and assistant director of the Comparative Oncology and Epigenetics Laboratory at the MU College of Veterinary Medicine, says this communication system can be used to “tell” cancer cells how to act, or even to die on command.

“During an infection, bacteria release molecules which allow them to ‘talk’ to each other,” said Kumar, the lead author of the study. “Depending on the type of molecule released, the signal will tell other bacteria to multiply, escape the immune system or even stop spreading. We found that if we introduce the ‘stop spreading’ bacteria molecule to cancer cells, those cells will not only stop spreading; they will begin to die as well.”

In the study published in PLOS ONE, Kumar, and co-author Jeffrey Bryan, an associate professor in the MU College of Veterinary Medicine, treated human pancreatic cancer cells grown in culture with bacterial communication molecules, known as ODDHSL. After the treatment, the pancreatic cancer cells stopped multiplying, failed to migrate and began to die.

“We used pancreatic cancer cells, because those are the most robust, aggressive and hard-to-kill cancer cells that can occur in the human body,” Kumar said. “To show that this molecule can not only stop the cancer cells from spreading, but actually cause them to die, is very exciting. Because this treatment shows promise in such an aggressive cancer like pancreatic cancer, we believe it could be used on other types of cancer cells and our lab is in the process of testing this treatment in other types of cancer.”

Kumar says the next step in his research is to find a more efficient way to introduce the molecules to the cancer cells before animal and human testing can take place.

“Our biggest challenge right now is to find a way to introduce these molecules in an effective way,” Kumar said. “At this time, we only are able to treat cancer cells with this molecule in a laboratory setting. We are now working on a better method which will allow us to treat animals with cancer to see if this therapy is truly effective. The early-stage results of this research are promising. If additional studies, including animal studies, are successful then the next step would be translating this application into clinics.”

Journal Reference:

  1. Ashwath S. Kumar, Jeffrey N. Bryan, Senthil R. Kumar. Bacterial Quorum Sensing Molecule N-3-Oxo-Dodecanoyl-L-Homoserine Lactone Causes Direct Cytotoxicity and Reduced Cell Motility in Human Pancreatic Carcinoma Cells.PLoS ONE, 2014; 9 (9): e106480 DOI: 10.1371/journal.pone.0106480