Arquivo da tag: Bactérias

Teamwork enables bacterial survival (Science Daily)

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 populationPNAS, 2016 DOI: 10.1073/pnas.1521056113
Anúncios

‘Nuvem personalizada’ de micróbios permite identificar indivíduos (Estadão)

FÁBIO DE CASTRO – O ESTADO DE S. PAULO

22 Setembro 2015 | 19h 02

Experimento realizado por cientistas americanos revela que cada pessoa lança ao ar milhões de bactérias por hora, formando ao seu redor uma combinação única de microorganismos

Cada pessoa traz em torno de si uma “nuvem personalizada” de micróbios e, de acordo com um novo estudo, é possível identificar um indivíduo a partir do exame da combinação única de bactérias suspensas no ar ao seu redor.

O novo estudo, liderado por pesquisadores da Universidade do Oregon, nos Estados Unidos, foi publicado hoje na revista científica Peerj.

De acordo com o estudo, cada pessoa lança ao ar, a cada hora, milhões de bactérias diferentesDe acordo com o estudo, cada pessoa lança ao ar, a cada hora, milhões de bactérias diferentes

A fim de testar até que ponto seres humanos possuem uma assinatura própria em suas nuvens de micróbios, os cientistas realizaram um experimento de sequenciamento genético dos micróbios suspenso no ar em torno de 11 pessoas diferentes.

Os voluntários foram colocados em câmaras experimentais higienizadas e, a partir do exame dos micróbios coletados no ar, os pesquisadores puderam identificar a maior parte deles a partir de suas combinações pessoais de bactérias.

Os micróbios que permitiram identificar os indivíduos são bactérias extremamente comuns – como a Streptococcus, normalmente encontrada na boca, a Propionibacterium e a Corynebacterium, ambas abundantes na pele humana.

Ainda que todos os micróbios tenham sido detectados no ar em torno de todos os voluntários do estudo, os autores descobriram que diferentes combinações das bactérias permitiam distinguir indivíduos.

“Nós já esperávamos que poderíamos detectar o conjunto de micróbios no ar em torno de uma pessoa, mas ficamos surpresos ao descobrir que podemos identificar a maior parte dos ocupantes das câmaras unicamente a partir de amostras de suas nuvens de micróbios”, disse o autor principal do estudo, James Meadow, pós-doutorando da Universidade do Oregon.

“Nossos resultados confirmam que um espaço ocupado é microbioticamente distinto de um espaço desocupado. Demonstramos também pela primeira vez que indivíduos emitem sua própria nuvem de micróbios personalizada”, afirmou Meadow.

“Aura” de micróbios. Durante o experimento, os voluntários receberam roupas limpas e foram isolados em uma câmara estéril, onde ficaram sentados em uma cadeira de plástico desinfetada por até quatro horas. As amostras das bactérias emitidas pelos indivíduos foi feita a partir de material coletado em placas de Petri – pequenos pratos de vidro usados em laboratório para culturas de bactérias – deixadas na câmara e em filtros de ar especiais.

Segundo Meadow, o exame do material deixou claro que cada voluntário emitiu milhões e milhões de micróbios pela respiração, pela pele e provavelmente pelo suor. Os cientistas verificaram que a combinação de bactérias de cada indivíduo era totalmente distinta.

O estudo, segundo os autores, ajuda a compreender até que ponto as pessoas emitem sua população específica de micróbios no ambiente ao redor e pode ajudar a entender os mecanismos envolvidos no alastramento de doenças infecciosas em prédios.

A descoberta pode ter também, de acordo com os autores, aplicações forenses como determinar onde uma pessoa esteve, embora ainda não tenha ficado claro se indivíduos podem ser detectados em um grupo com muitas pessoas.

Small advances: understanding the micro biome (ABC RN)

Tuesday 1 September 2015 4:27PM

Amanda Smith

Microbes

IMAGE: THE HUMAN MICROBIOME MAY PLAY A ROLE IN EVERYTHING FROM OBESITY TO ASTHMA (FLICKR/PACIFIC NORTHWEST NATIONAL LABORATORY)

What is it that makes you, you? While you’re made up of 10 trillion human cells, 100 trillion microbial cells also live on you and in you. This vast array of microscopic bugs may be your defining feature, and scientists around the world are racing to find out more. Amanda Smith reports.

AUDIO: https://soundcloud.com/abc_rn/excerpt-the-body-microbial/s-oz6JA

Microbes, it seems, are the next big thing. Around the world, scientists are researching the human microbiome—the genes of our microbes—in the hope of unlocking quite a different way to understand sickness and health.

At the Microbiome Initiative at the University of California, San Diego, Rob Knight runs the American Gut Project, a citizen science initiative where you can get your microbiome sequenced.

Breast milk is meant to present the baby with a manageable dose of everything in the environment. It samples the entire environment—everything the mother eats, breathes, touches.

MAUREEN MINCHIN, AUTHOR OF MILK MATTERS.

‘What we can do right now is put you on this microbial map, where we can compare your microbes to the microbes of thousands of other people we’ve already looked at,’ he says. ‘But what we need to do is develop more of a microbial GPS that doesn’t just tell you where you are, but tells you where you want to go and what you need to do, step by step, in order to get there.’

The Australian Centre for Ecogenomics is also setting up a service where you can get your gut microbes analysed. The centre’s director, Phillip Hugenholtz, predicts that in years to come such a process will be a diagnostic procedure when you go to the doctor, much like getting a blood test.

‘I definitely think that’s going to become a standard part of your personalised medicine’, he says. ‘Micro-organisms are sometimes a very good early indicator of things occurring in your body and so it will become something that you’d go and get done maybe once or twice a year to see what’s going on.’

While this level of interest in the microbiome is new, the first person to realise we’re all teeming with micro-organisms was Dutchman Anton Leeuwenhoek, way back in 1676. Leeuwenhoek was interested in making lenses, and constructed himself a microscope.

‘He was looking at the scum from his teeth, and was amazed to see in this scraped-off plaque from inside his own mouth what he called hundreds of different “animalcules swimming a-prettily”,’ says Tim Spector, professor of genetic epidemiology at Kings College London.

‘He was the first to describe this, and it took hundreds of years before people actually believed that we were completely full of these microbes and we’d co-evolved with them.’

Microbes have come a long way over the last century. Until recent advances in DNA sequencing, all tummy bugs were considered bad.

‘We used to think that there was no such thing as a good microbe in our guts, that they were all out to do us no good, and we’ve basically spent the last 100 years trying to eliminate them with disinfectants and then the last 50 years with antibiotics,’ says Spector.

This has given rise to the ‘hygiene hypothesis’, which contends that by keeping ourselves too clean, we’re denying ourselves the microbes necessary to keep our immune system balanced, resulting in all sorts of chronic diseases.

‘Over the last half-century, as infectious diseases like polio and measles and hepatitis and so-on have plummeted in their frequency, chronic diseases—everything from obesity to diabetes to inflammatory bowel disease—have been skyrocketing,’ says the Microbiome Initiative’s Rob Knight.

‘So the idea is that potentially without exposure to a diverse range of healthy microbes our immune systems might be going into overdrive and attacking our own cells, or overreacting to harmless things we find in the environment.’

Antonie van Leeuwenhoek

IMAGE: ANTONIE VAN LEEUWENHOEK WAS THE FIRST MICROBIOLOGIST AND THE FIRST TO OBSERVE MICRO-ORGANISMS USING A MICROSCOPE. (LICENSED UNDER PUBLIC DOMAIN VIA COMMONS)

In terms of human DNA, we’re all 99.99 per cent identical. However our microbial profiles can differ enormously. We might share just 10 per cent of our dominant microbial species with others.

According to Knight, some of the differences are explained by method of birth.

‘If you come out the regular way you get coated with microbes as you’re passing through your mother’s birth canal,’ he says.

Babies delivered by Caesarian section, on the other hand, have microbes that are mostly found on adult skin, from being touched by different doctors and nurses.

‘One thing that’s potentially interesting about that is differences between C-section and vaginally delivered babies have been reported: higher rates in C-section babies of asthma, allergies, atopic disease, even obesity. All of those have been linked to the microbiome now.’

Also important to the development of healthy microbiota in babies is breastfeeding, according to Maureen Minchin, the author of Milk Matters.

‘We’ve known for over 100 years that breast milk and formula result in very, very different gut flora in babies, but it’s only very recently that anyone has thought to look and see what breast milk does contain, and at last count there were well over 700 species of bacteria in breast milk,’ she says.

According to Minchin, breastfeeding is the bridge between the womb and the world for babies.

‘Breast milk is meant to present the baby with a manageable dose of everything in the environment. It samples the entire environment—everything the mother eats, breathes, touches. Her microbiome is present in that breast milk and will help create the appropriate microbiome in the baby.’

Minchin is an advocate of the World Health Organisation’s recommendation to breastfeed exclusively to six months and then continue breastfeeding while introducing other foods through the first and second year.

Related: Why the digestive system and its bacteria are a ‘second brain’

So if what babies are fed is important for their microbiome, what about adults? Tim Spector says research into microbes is yielding new information about healthy eating.

‘It’s going to soon revolutionise how we look at food and diet. This is one of the most exciting things in science at the moment, because it’s obviously much easier to change your microbes than it is to change your genes.’

‘Most processed foods only contain about five ingredients, and in a way our epidemic of the last 30 years of obesity and allergy is that our diets have become less and less diverse.’

According to Spector, studies of people with various chronic diseases, obesity and diabetes show a common feature, which is that their gut microbes have a much-reduced diversity compared to healthy people.

He likes to use the analogy of a garden: ‘A neglected garden has very few species, not much fertilised soil, and this allows weeds to take over in great numbers,’ he says.

‘I think this is a nice concept because we’re very good gardeners, humans, and I think we need to start using those principles—fertilising, adding soil, experimenting and avoiding adding nasty toxins to our own bodies as we would our gardens.’

May your gut flora bloom!

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

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.

Gut microbiota influences blood-brain barrier permeability (Science Daily)

Date: November 19, 2014

Source: Karolinska Institutet

Summary: Our natural gut-residing microbes can influence the integrity of the blood-brain barrier, which protects the brain from harmful substances in the blood, a new study in mice shows. The blood-brain barrier is a highly selective barrier that prevents unwanted molecules and cells from entering the brain from the bloodstream.


Uptake of the substance Raclopride in the brain of germ-free versus conventional mice. Credit: Miklos Toth

A new study in mice, conducted by researchers at Sweden’s Karolinska Institutet together with colleagues in Singapore and the United States, shows that our natural gut-residing microbes can influence the integrity of the blood-brain barrier, which protects the brain from harmful substances in the blood. According to the authors, the findings provide experimental evidence that our indigenous microbes contribute to the mechanism that closes the blood-brain barrier before birth. The results also support previous observations that gut microbiota can impact brain development and function.

The blood-brain barrier is a highly selective barrier that prevents unwanted molecules and cells from entering the brain from the bloodstream. In the current study, being published in the journal Science Translational Medicine, the international interdisciplinary research team demonstrates that the transport of molecules across the blood-brain barrier can be modulated by gut microbes — which therefore play an important role in the protection of the brain.

The investigators reached this conclusion by comparing the integrity and development of the blood-brain barrier between two groups of mice: the first group was raised in an environment where they were exposed to normal bacteria, and the second (called germ-free mice) was kept in a sterile environment without any bacteria.

“We showed that the presence of the maternal gut microbiota during late pregnancy blocked the passage of labeled antibodies from the circulation into the brain parenchyma of the growing fetus,” says first author Dr. Viorica Braniste at the Department of Microbiology, Tumor and Cell Biology at Karolinska Institutet. “In contrast, in age-matched fetuses from germ-free mothers, these labeled antibodies easily crossed the blood-brain barrier and was detected within the brain parenchyma.”

The team also showed that the increased ‘leakiness’ of the blood-brain barrier, observed in germ-free mice from early life, was maintained into adulthood. Interestingly, this ‘leakiness’ could be abrogated if the mice were exposed to fecal transplantation of normal gut microbes. The precise molecular mechanisms remain to be identified. However, the team was able to show that so-called tight junction proteins, which are known to be important for the blood-brain barrier permeability, did undergo structural changes and had altered levels of expression in the absence of bacteria.

According to the researchers, the findings provide experimental evidence that alterations of our indigenous microbiota may have far-reaching consequences for the blood-brain barrier function throughout life.

“These findings further underscore the importance of the maternal microbes during early life and that our bacteria are an integrated component of our body physiology,” says Professor Sven Pettersson, the principal investigator at the Department of Microbiology, Tumor and Cell Biology. “Given that the microbiome composition and diversity change over time, it is tempting to speculate that the blood-brain barrier integrity also may fluctuate depending on the microbiome. This knowledge may be used to develop new ways for opening the blood-brain-barrier to increase the efficacy of the brain cancer drugs and for the design of treatment regimes that strengthens the integrity of the blood-brain barrier.”


Journal Reference:

  1. V. Braniste, M. Al-Asmakh, C. Kowal, F. Anuar, A. Abbaspour, M. Toth, A. Korecka, N. Bakocevic, N. L. Guan, P. Kundu, B. Gulyas, C. Halldin, K. Hultenby, H. Nilsson, H. Hebert, B. T. Volpe, B. Diamond, S. Pettersson. The gut microbiota influences blood-brain barrier permeability in miceScience Translational Medicine, 2014; 6 (263): 263ra158 DOI: 10.1126/scitranslmed.3009759

How the bacteria in our gut affect our cravings for food (Conversation)

November 6 2014, 10.00pm EST

Vincent Ho

Gut bacteria can manufacture special proteins that are very similar to hunger-regulating hormones. Lighthunter/Shutterstock

We’ve long known that that the gut is responsible for digesting food and expelling the waste. More recently, we realised the gut has many more important functions and acts a type of mini-brain, affecting our mood and appetite. Now, new research suggests it might also play a role in our cravings for certain types of food.

How does the mini-brain work?

The gut mini-brain produces a wide range of hormones and contains many of the same neurotransmitters as the brain. The gut also contains neurons that are located in the walls of the gut in a distributed network known as the enteric nervous system. In fact, there are more of these neurons in the gut than in the entire spinal cord.

The enteric nervous system communicates to the brain via the brain-gut axis and signals flow in both directions. The brain-gut axis is thought to be involved in many regular functions and systems within the healthy body, including the regulation of eating.

Let’s consider what happens to the brain-gut axis when we eat a meal. When food arrives in the stomach, certain gut hormones are secreted. These activate signalling pathways from the gut to the brainstem and the hypothalamus to stop food consumption. Such hormones include the appetite-suppressing hormones peptide YY and cholecystokinin.

Gut hormones can bind and activate receptor targets in the brain directly but there is strong evidence that the vagus nerve plays a major role in brain-gut signalling. The vagus nerve acts as a major highway in the brain-gut axis, connecting the over 100 million neurons in the enteric nervous system to the medulla (located at the base of the brain).

Research has shown that vagus nerve blockade can lead to marked weight loss, while vagus nerve stimulation is known to trigger excessive eating in rats.

This brings us to the topic of food cravings. Scientists have largely debunked the myth that food cravings are our bodies’ way of letting us know that we need a specific type of nutrient. Instead, an emerging body of research suggests that our food cravings may actually be significantly shaped by the bacteria that we have inside our gut. In order to explore this further we will cover the role of gut microbes.

Gut microbiota

As many as 90% of our cells are bacterial. In fact, bacterial genes outnumber human genes by a factor of 100 to one.

The gut is an immensely complex microbial ecosystem with many different species of bacteria, some of which can live in an oxygen-free environment. An average person has approximately 1.5 kilograms of gut bacteria. The term “gut microbiota” is used to describe the bacterial collective.

We each have around 1.5kg of bacteria in our guts. Christopher PooleyCC BY

Gut microbiota send signals to the brain via the brain-gut axis and can have dramatic effects on animal behaviour and health.

In one study, for example, mice that were genetically predisposed to obesity remained lean when they were raised in a sterile environment without gut microbiota. These germ-free mice were, however, transformed into obese mice when fed a faecal pellet that came from an obese mouse raised conventionally.

The role of gut microbiota in food cravings

There is growing evidence to support the role of gut microbiota in influencing why we crave certain foods.

We know that mice that are bred in germ-free environments prefer more sweets and have greater number of sweet taste receptors in their gut compared to normal mice. Research has also found that persons who are “chocolate desiring” have microbial breakdown products in their urine that are different from those of “chocolate indifferent individuals” despite eating identical diets.

Many gut bacteria can manufacture special proteins (called peptides) that are very similar to hormones such as peptide YY and ghrelin that regulate hunger. Humans and other animals have produced antibodies against these peptides. This raises the distinct possibility that microbes might be able to directly influence human eating behaviour through their peptides that mimic hunger-regulating hormones or indirectly through antibodies that can interfere with appetite regulation.

Practical implications

There are substantial challenges to overcome before we can apply this knowledge about gut microbiota in a practical sense.

First, there is the challenge of collecting the gut microbes. Traditionally this is collected from stools but gut microbiota is known to vary between different regions of the gut, such as the small intestine and colon. Obtaining bacterial tissue through endoscopy or another invasive collection technique in addition to stool samples may lead to more accurate representation of the gut microbiome.

Second, the type of sequencing that is currently used for gut microbiota screening is expensive and time-consuming. Advances will need to be made before this technology is in routine use.

Probably the greatest challenge in gut microbiota research is the establishment of a strong correlation between gut microbiota patterns and human disease. The science of gut microbiota is in its infancy and there needs to be much more research mapping out disease relationships.

Probiotics contain live microorganisms. Quanthem/Shutterstock

But there is reason to be hopeful. There is now strong interest in utilising both prebiotics and probiotics to alter our gut micro biome. Prebiotics are non-digestible carbohydrates that trigger the growth of beneficial gut bacteria, while probiotics are beneficial live microorganisms contained in foods and supplements.

Faecal transplantation is also now an accepted treatment for those patients that have a severe form of gut bacterial infection called Clostridium difficile, which has been unresponsive to antibiotics.

The use of such targeted strategies is likely to become increasingly common as we better understand how gut microbiota influence our bodily functions, including food cravings.

Bactéria pode ter sistema imune rudimentar, indica estudo (Fapesp)

03 de outubro de 2014

Por Karina Toledo

Agência FAPESP – Um estudo publicado na revista Nature Communications revelou que a bactéria Salmonella enterica é capaz de produzir uma proteína muito semelhante à alfa-2-macroglobulina humana, que desempenha um papel-chave em nosso sistema imunológico.

A hipótese levantada pelos pesquisadores do Instituto de Biologia Estrutural (IBS) de Grenoble, na França, é de que também nas bactérias as macroglobulinas poderiam fazer parte de um sistema de defesa rudimentar. Se a teoria for confirmada por estudos futuros, essas proteínas podem se tornar alvos para o desenvolvimento de novos antibióticos.

“O mais fascinante é que as macroglobulinas são proteínas imensas, formadas por quase 1.700 resíduos de aminoácidos. Para a bactéria sintetizar uma molécula tão grande é porque ela deve ter um papel muito importante”, afirmou a brasileira Andréa Dessen, pesquisadora do IBS e coordenadora, no Laboratório Nacional de Biociência (LNBio), em Campinas, de um projeto apoiado pela FAPESP por meio do programa São Paulo Excellence Chairs (SPEC).

No organismo humano, a missão da alfa-2-macroglobulina é detectar e neutralizar proteases secretadas por microrganismos invasores, disse a pesquisadora. As proteases são enzimas que quebram as ligações entre os aminoácidos das proteínas.

“A macroglobulina impede, dessa forma, que as proteases dos invasores destruam os tecidos do organismo, o que permitiria a infecção de tecidos mais profundos”, explicou.

Além disso, a alfa-2-macroglobulina também se liga a proteases que participam do processo de coagulação sanguínea, evitando que proteínas importantes sejam destruídas indevidamente.

Em estudos anteriores, nos quais o genoma de diversas espécies de bactérias foi sequenciado, pesquisadores alemães já haviam observado a presença do gene da macroglobulina. No IBS, o grupo liderado por Dessen já havia feito a caracterização bioquímica da proteína produzida pelas espécies Escherichia coli e Pseudomonas aeruginosa.

“Agora, de maneira inédita, estudamos a estrutura tridimensional da macroglobulina secretada pela Salmonella enterica por uma técnica conhecida como cristalografia de raios X, que permite visualizar detalhes em nível atômico. E pudemos confirmar que, de fato, ela é muito parecida com a macroglobulina humana”, contou Dessen.

De acordo com a pesquisadora, a descoberta reforça a hipótese de que a alfa-2-macroglobulina tem o papel de proteger a bactéria das proteases secretadas por outras bactérias ou pelo organismo do hospedeiro que ela tenta infectar.

“Em um modelo de camundongo, pesquisadores canadenses mostraram que cepas da bactéria Pseudomonas aeruginosa que não produzem macroglobulina têm menor capacidade de causar doença, ou seja, são menos virulentas. A proteína parece dar uma vantagem à bactéria na hora de colonizar o hospedeiro, mas ainda não sabemos exatamente por quê”, disse.

Desdobramentos

Em um braço da pesquisa que está sendo conduzido no LNBio, com apoio da FAPESP e orientação de Dessen, a pós-doutoranda francesa Samira Zouhir investiga a estrutura da macroglobulina sintetizada por bactérias da espécie Pseudomonas aeruginosa – causadora de diversos casos de infecção hospitalar.

“Se conseguirmos desvendar a estrutura tridimensional da proteína, isso nos dará pistas sobre sua função no processo infeccioso”, disse Dessen.

Quando o papel das macroglobulinas estiver bem compreendido em diferentes espécies de bactérias, acrescentou, essas proteínas poderão se tornar alvo para o desenvolvimento de novos antibióticos.

“Também há pesquisas interessantes em modelo de camundongo mostrando que a aplicação de alfa-globulina humana pode oferecer proteção contra a sepse. Há várias possibilidades de tratamento a serem exploradas”, avaliou a pesquisadora.

O artigo Structure of a bacterial α2-macroglobulin reveals mimicry of eukaryotic innate immunity (doi: 10.1038/ncomms5917), pode ser lido em www.nature.com/ncomms/2014/140915/ncomms5917/full/ncomms5917.html.

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

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

Certain gut bacteria may induce metabolic changes following exposure to artificial sweeteners (Science Daily)

Date: September 17, 2014

Source: Weizmann Institute of Science

Summary: Artificial sweeteners have long been promoted as diet and health aids. But breaking research shows that these products may be leading to the very diseases they were said to help prevent: scientists have discovered that, after exposure to artificial sweeteners, our gut bacteria may be triggering harmful metabolic changes.


This image depicts gut microbiota. Credit: Weizmann Institute of Science

Artificial sweeteners — promoted as aids to weight loss and diabetes prevention — could actually hasten the development of glucose intolerance and metabolic disease, and they do so in a surprising way: by changing the composition and function of the gut microbiota — the substantial population of bacteria residing in our intestines. These findings, the results of experiments in mice and humans, were published September 17 in Nature. Dr. Eran Elinav of the Weizmann Institute of Science’s Department of Immunology, who led this research together with Prof. Eran Segal of the Department of Computer Science and Applied Mathematics, says that the widespread use of artificial sweeteners in drinks and food, among other things, may be contributing to the obesity and diabetes epidemic that is sweeping much of the world.

For years, researchers have been puzzling over the fact that non-caloric artificial sweeteners do not seem to assist in weight loss, with some studies suggesting that they may even have an opposite effect. Graduate student Jotham Suez in Dr. Elinav’s lab, who led the study, collaborated with lab member Gili Zilberman-Shapira and graduate students Tal Korem and David Zeevi in Prof. Segal’s lab to discover that artificial sweeteners, even though they do not contain sugar, nonetheless have a direct effect on the body’s ability to utilize glucose. Glucose intolerance — generally thought to occur when the body cannot cope with large amounts of sugar in the diet — is the first step on the path to metabolic syndrome and adult-onset diabetes.

The scientists gave mice water laced with the three most commonly used artificial sweeteners, in amounts equivalent to those permitted by the U.S. Food and Drug Administration (FDA). These mice developed glucose intolerance, as compared to mice that drank water, or even sugar water. Repeating the experiment with different types of mice and different doses of the artificial sweeteners produced the same results — these substances were somehow inducing glucose intolerance.

Next, the researchers investigated a hypothesis that the gut microbiota are involved in this phenomenon. They thought the bacteria might do this by reacting to new substances like artificial sweeteners, which the body itself may not recognize as “food.” Indeed, artificial sweeteners are not absorbed in the gastrointestinal tract, but in passing through they encounter trillions of the bacteria in the gut microbiota.

The researchers treated mice with antibiotics to eradicate many of their gut bacteria; this resulted in a full reversal of the artificial sweeteners’ effects on glucose metabolism. Next, they transferred the microbiota from mice that consumed artificial sweeteners to “germ-free,” or sterile, mice — resulting in a complete transmission of the glucose intolerance into the recipient mice. This, in itself, was conclusive proof that changes to the gut bacteria are directly responsible for the harmful effects to their host’s metabolism. The group even found that incubating the microbiota outside the body, together with artificial sweeteners, was sufficient to induce glucose intolerance in the sterile mice. A detailed characterization of the microbiota in these mice revealed profound changes to their bacterial populations, including new microbial functions that are known to infer a propensity to obesity, diabetes, and complications of these problems in both mice and humans.

Does the human microbiome function in the same way? Dr. Elinav and Prof. Segal had a means to test this as well. As a first step, they looked at data collected from their Personalized Nutrition Project (www.personalnutrition.org), the largest human trial to date to look at the connection between nutrition and microbiota. Here, they uncovered a significant association between self-reported consumption of artificial sweeteners, personal configurations of gut bacteria, and the propensity for glucose intolerance. They next conducted a controlled experiment, asking a group of volunteers who did not generally eat or drink artificially sweetened foods to consume them for a week, and then undergo tests of their glucose levels and gut microbiota compositions.

The findings showed that many — but not all — of the volunteers had begun to develop glucose intolerance after just one week of artificial sweetener consumption. The composition of their gut microbiota explained the difference: the researchers discovered two different populations of human gut bacteria — one that induced glucose intolerance when exposed to the sweeteners, and one that had no effect either way. Dr. Elinav believes that certain bacteria in the guts of those who developed glucose intolerance reacted to the chemical sweeteners by secreting substances that then provoked an inflammatory response similar to sugar overdose, promoting changes in the body’s ability to utilize sugar.

Prof. Segal states, “The results of our experiments highlight the importance of personalized medicine and nutrition to our overall health. We believe that an integrated analysis of individualized ‘big data’ from our genome, microbiome, and dietary habits could transform our ability to understand how foods and nutritional supplements affect a person’s health and risk of disease.”

According to Dr. Elinav, “Our relationship with our own individual mix of gut bacteria is a huge factor in determining how the food we eat affects us. Especially intriguing is the link between use of artificial sweeteners — through the bacteria in our guts — to a tendency to develop the very disorders they were designed to prevent; this calls for reassessment of today’s massive, unsupervised consumption of these substances.”

Journal Reference:

  1. Jotham Suez, Tal Korem, David Zeevi, Gili Zilberman-Schapira, Christoph A. Thaiss, Ori Maza, David Israeli, Niv Zmora, Shlomit Gilad, Adina Weinberger, Yael Kuperman, Alon Harmelin, Ilana Kolodkin-Gal, Hagit Shapiro, Zamir Halpern, Eran Segal, Eran Elinav. Artificial sweeteners induce glucose intolerance by altering the gut microbiota. Nature, 2014; DOI: 10.1038/nature13793

Gut bacteria that protect against food allergies identified (Science Daily)

Date: August 25, 2014

Source: University of Chicago Medical Center

Summary: The presence of Clostridia, a common class of gut bacteria, protects against food allergies, a new study in mice finds. The discovery points toward probiotic therapies for this so-far untreatable condition. Food allergies affect 15 million Americans, including one in 13 children, who live with this potentially life-threatening disease that currently has no cure, researchers note.

Artist’s rendering of bacteria (stock illustration). Credit: © zuki70 / Fotolia

The presence of Clostridia, a common class of gut bacteria, protects against food allergies, a new study in mice finds. By inducing immune responses that prevent food allergens from entering the bloodstream, Clostridia minimize allergen exposure and prevent sensitization — a key step in the development of food allergies. The discovery points toward probiotic therapies for this so-far untreatable condition, report scientists from the University of Chicago, Aug 25 in the Proceedings of the National Academy of Sciences.

Although the causes of food allergy — a sometimes deadly immune response to certain foods — are unknown, studies have hinted that modern hygienic or dietary practices may play a role by disturbing the body’s natural bacterial composition. In recent years, food allergy rates among children have risen sharply — increasing approximately 50 percent between 1997 and 2011 — and studies have shown a correlation to antibiotic and antimicrobial use.

“Environmental stimuli such as antibiotic overuse, high fat diets, caesarean birth, removal of common pathogens and even formula feeding have affected the microbiota with which we’ve co-evolved,” said study senior author Cathryn Nagler, PhD, Bunning Food Allergy Professor at the University of Chicago. “Our results suggest this could contribute to the increasing susceptibility to food allergies.”

To test how gut bacteria affect food allergies, Nagler and her team investigated the response to food allergens in mice. They exposed germ-free mice (born and raised in sterile conditions to have no resident microorganisms) and mice treated with antibiotics as newborns (which significantly reduces gut bacteria) to peanut allergens. Both groups of mice displayed a strong immunological response, producing significantly higher levels of antibodies against peanut allergens than mice with normal gut bacteria.

This sensitization to food allergens could be reversed, however, by reintroducing a mix of Clostridia bacteria back into the mice. Reintroduction of another major group of intestinal bacteria, Bacteroides, failed to alleviate sensitization, indicating that Clostridia have a unique, protective role against food allergens.

Closing the door

To identify this protective mechanism, Nagler and her team studied cellular and molecular immune responses to bacteria in the gut. Genetic analysis revealed that Clostridia caused innate immune cells to produce high levels of interleukin-22 (IL-22), a signaling molecule known to decrease the permeability of the intestinal lining.

Antibiotic-treated mice were either given IL-22 or were colonized with Clostridia. When exposed to peanut allergens, mice in both conditions showed reduced allergen levels in their blood, compared to controls. Allergen levels significantly increased, however, after the mice were given antibodies that neutralized IL-22, indicating that Clostridia-induced IL-22 prevents allergens from entering the bloodstream.

“We’ve identified a bacterial population that protects against food allergen sensitization,” Nagler said. “The first step in getting sensitized to a food allergen is for it to get into your blood and be presented to your immune system. The presence of these bacteria regulates that process.” She cautions, however, that these findings likely apply at a population level, and that the cause-and-effect relationship in individuals requires further study.

While complex and largely undetermined factors such as genetics greatly affect whether individuals develop food allergies and how they manifest, the identification of a bacteria-induced barrier-protective response represents a new paradigm for preventing sensitization to food. Clostridia bacteria are common in humans and represent a clear target for potential therapeutics that prevent or treat food allergies. Nagler and her team are working to develop and test compositions that could be used for probiotic therapy and have filed a provisional patent.

“It’s exciting because we know what the bacteria are; we have a way to intervene,” Nagler said. “There are of course no guarantees, but this is absolutely testable as a therapeutic against a disease for which there’s nothing. As a mom, I can imagine how frightening it must be to worry every time your child takes a bite of food.”

“Food allergies affect 15 million Americans, including one in 13 children, who live with this potentially life-threatening disease that currently has no cure,” said Mary Jane Marchisotto, senior vice president of research at Food Allergy Research & Education. “We have been pleased to support the research that has been conducted by Dr. Nagler and her colleagues at the University of Chicago.”


Journal Reference:

  1. A. T. Stefka, T. Feehley, P. Tripathi, J. Qiu, K. McCoy, S. K. Mazmanian, M. Y. Tjota, G.-Y. Seo, S. Cao, B. R. Theriault, D. A. Antonopoulos, L. Zhou, E. B. Chang, Y.-X. Fu, C. R. Nagler. Commensal bacteria protect against food allergen sensitization. Proceedings of the National Academy of Sciences, 2014; DOI: 10.1073/pnas.1412008111

Bactéria pode aumentar inteligência (Exame)

Microbiologia | 24/05/2010 15:50

Cientistas acreditam que espécie também tem capacidades antidepressivas por aumentar níveis de serotonina no cérebro

Célio Yano 

São Paulo – Uma espécie de bactéria que os cientistas já acreditavam ter capacidades antidepressivas pode também deixar pessoas mais inteligentes. A descoberta foi apresentada hoje no 110º Encontro Geral da Sociedade Americana de Microbiologia (ASM, na sigla em inglês), realizado em San Diego, nos Estados Unidos.

“A Mycobacterium vaccae é uma bactéria de solo natural, que as pessoas geralmente ingerem ou respiram quando passam algum tempo na natureza”, disse Dorothy Matthews, que conduziu a pesquisa junto com Susan Jenks. Espécie não-patogênica, a M. vaccae tem esse nome por ter sido encontrada pela primeira vez em fezes de vaca.

De acordo com a ASM, estudos anteriores já haviam mostrado que bactérias da espécie mortas injetadas em ratos estimulam o crescimento de alguns neurônios que resultam no aumento de níveis de serotonina e reduzem a ansiedade.

Como a serotonina, tipo de neurotransmissor, desempenha um papel importante no aprendizado, Dorothy e Susan imaginaram que a M. vaccae vivas poderiam aumentar a capacidade de aprendizado do rato. Elas então alimentaram as cobaias com bactérias vivas e testaram a habilidade dos roedores para percorrer um labirinto. Conforme as pesquisadoras, os ratos que se alimentaram da bactéria atravessaram o labirinto duas vezes mais rápido e com menor índice de ansiedade que ratos que não haviam recebido o tratamento.

Em um segundo experimento, as bactérias foram removidas da dieta dos animais e eles foram testados novamente. Embora os ratos percorressem o labirinto mais lentamente do que haviam feito quando ingeriram a bactéria, eles ainda eram mais rápidos que os ratos que não haviam ingerido M. vaccae em nenhum momento. Após três semanas de descanso, os ratos ainda percorriam o labirinto mais rapidamente que os demais, mas os resultados já não eram mais estatisticamente significantes, o que sugere que o efeito foi temporário.

“Esta pesquisa mostra que M. vaccae pode ter uma função na ansiedade e aprendizado de mamíferos”, disse Dorothy. “É interessante imaginarmos que criar ambientes de aprendizado nas escolas que incluam momentos ao ar livre, onde M. vaccae esteja presente, pode baixar a ansiedade e aumentar a capacidade de aprender novas tarefas”, complementou.

Life-style determines gut microbes (Max-Planck-Gesellschaft)

An international team of researchers has for the first time deciphered the intestinal bacteria of present-day hunter-gatherers

April 15, 2014

The gut microbiota is responsible for many aspects of human health and nutrition, but most studies have focused on “western” populations. An international collaboration of researchers, including researchers of the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, has for the first time analysed the gut microbiota of a modern hunter-gatherer community, the Hadza of Tanzania. The results of this work show that Hadza harbour a unique microbial profile with features yet unseen in any other human group, supporting the notion that Hadza gut bacteria play an essential role in adaptation to a foraging subsistence pattern. The study further shows how gut microbiota may have helped our ancestors adapt and survive during the Paleolithic.

Hadza women roasting tubers.
Hadza women roasting tubers. © Alyssa Crittenden

Bacterial populations have co-evolved with humans over millions of years, and have the potential to help us adapt to new environments and foods. Studies of the Hadza offer an especially rare opportunity for scientists to learn how humans survive by hunting and gathering, in the same environment and using similar foods as our ancestors did.

The research team, composed of anthropologists, microbial ecologists, molecular biologists, and analytical chemists, and led in part by Stephanie Schnorr and Amanda Henry of the Max Planck Institute for Evolutionary Anthropology, compared the Hadza gut microbiota to that of urban living Italians, representative of a “westernized” population. Their results, published recently in Nature Communications, show that the Hadza have a more diverse gut microbe ecosystem, i.e. more bacterial species compared to the Italians. “This is extremely relevant for human health”, says Stephanie Schnorr. “Several diseases emerging in industrialized countries, like IBS, colorectal cancer, obesity, type II diabetes, Crohn’s disease and others, are significantly associated with a reduction in gut microbial diversity.”

The Hadza gut microbiota is well suited for processing indigestible fibres from a plant-rich diet and likely helps the Hadza get more energy from the fibrous foods that they consume. Surprisingly, Hadza men and women differed significantly in the type and amount of their gut microbiota, something never before seen in any other human population. Hadza men hunt game and collect honey, while Hadza women collect tubers and other plant foods. Though they share these foods, each sex eats slightly more of the foods they target. “The differences in gut microbiota between the sexes reflects this sexual division of labour”, says Stephanie Schnorr. “It appears that women have more bacteria to help process fibrous plant foods, which has direct implications for their fertility and reproductive success.” These findings support the key role of the gut microbiota as adaptive partners during the course of human evolution by aligning with differing diets.

Hadza digging for plant foods.Hadza digging for plant foods. © MPI f. Evolutionary Anthropology

Finally, the Hadza gut microbe community is a unique configuration with high levels of bacteria, like Treponema, that in western populations are often considered signs of disease, and low levels of other bacteria, likeBifidobacterium, that in western populations are considered “healthy”. However, the Hadza experience little to no autoimmune diseases that would result from gut bacteria imbalances. Therefore, we must redefine our notions of “healthy” and “unhealthy” bacteria, since these distinctions are clearly dependent on the environment we live in. Genetic diversity of bacteria is likely the most important criterion for the health and stability of the gut microbiome.

“Co-resident microbes are our ‘old friends’ that help us adapt to different lifestyles and environments”, says Amanda Henry, leader of the Max Planck Research Group on Plant Foods in Hominin Dietary Ecology. “Through this analysis of the Hadza gut microbiota, we have increased our knowledge of human-microbiome adaptations to life in a savanna environment and improved our understanding of how gut microbiota may have helped our ancestors adapt and survive during the Paleolithic.”

Gene Variants in Immune System Pathways Correlated With Composition of Microbes of Human Body (Science Daily)

Oct. 24, 2013 — Human genes in immunity-related pathways are likely associated with the composition of an individual’s microbiome, which refers to the bacteria and other microbes that live in and on the body, scientists reported today, Oct. 24, at the American Society of Human Genetics 2013 annual meeting in Boston.

Bacterial colonies on an agar plate. This study is the first genome-wide and microbiome-wide investigation to identify the interactions between human genetic variation and the composition of the microbes that inhabit the human body. (Credit: © anyaivanova / Fotolia)

“These genes are significantly enriched in inflammatory and immune pathways and form an interaction network highly enriched with immunity-related functions,” said Ran Blekhman, Ph.D., Assistant Professor, Department of Genetics, Cell Biology, and Development at the University of Minnesota, Minneapolis.

The study is the first genome-wide and microbiome-wide investigation to identify the interactions between human genetic variation and the composition of the microbes that inhabit the human body.

The skin, genital areas, mouth, and other areas of the human body, especially the intestines, are colonized by trillions of bacteria and other microorganisms. “Shifts in the composition of the species of the microbes have been associated with multiple chronic conditions, such as diabetes, inflammatory bowel disease and obesity,” noted Dr. Blekhman.

Dr. Blekhman and his collaborators found evidence of genetic influences on microbiome composition at 15 body sites of 93 people surveyed. “We found in our study that genetic variation correlated with the microbiome at two levels,” he said.

At the individual level, the mathematical procedure known as principal component analysis demonstrated that genetic variation correlated with the overall structure of a person’s microbiome.

At the species level, potential correlations between host genetic variation and the abundance of a single bacterial species were identified, said Dr. Blekhman, who conducted much of the research while a scientist in the lab of Andrew G. Clark, Ph.D., the Jacob Gould Schurman Professor of Population Genetics in the Department of Molecular Biology and Genetics at Cornell University, Ithaca, NY. Dr. Clark is the senior author of the abstract.

To identify the bacterial species that inhabited each human body site, the researchers mined sequence data from the Human Microbiome Project (HMP), an international program to genetically catalog the microbial residents of the human body.

Using a systems-level association approach, the researchers showed that variation in genes related to immune system pathways was correlated with microbiome composition in the 15 host body sites.

To shed light on the evolutionary history of the symbiosis between humans and their microbiomes, the researchers analyzed sequencing data from the 1000 Genomes Project, which is designed to provide a comprehensive resource on human genetic variation.

They found that the genes in the pathways linked to the composition of an individual’s microbiome vary significantly across populations. “Moreover, many of those genes have been shown in recent studies to be under selective pressure,” said Dr. Blekhman.

“The results highlight the role of host immunity in determining bacteria levels across the body and support a possible role for the microbiome in driving the evolution of bacteria-associated host genes,” he added.

Dr. Blekhman is currently investigating the combined role of host genetics and the microbiome in influencing an individual’s susceptibility to such diseases as colon cancer. His goal is to unravel the interaction between host genomic variation and the gut microbiome in colon cancer incidence, evolution and therapeutic response.

No Idle Chatter: Malaria Parasites ‘Talk’ to Each Other (Science Daily)

May 15, 2013 — Melbourne scientists have made the surprise discovery that malaria parasites can ‘talk’ to each other — a social behaviour to ensure the parasite’s survival and improve its chances of being transmitted to other humans.

Professor Alan Cowman (left) and Dr Neta Regev-Rudzki have made the surprise discovery that malaria parasites can ‘talk’ to each other. This social behaviour ensures the parasite’s survival and improves its chances of being transmitted to other humans. (Credit: Image courtesy of Walter and Eliza Hall Institute)

The finding could provide a niche for developing antimalarial drugs and vaccines that prevent or treat the disease by cutting these communication networks.

Professor Alan Cowman, Dr Neta Regev-Rudzki, Dr Danny Wilson and colleagues from the Walter and Eliza Hall Institute’s Infection and Immunity division, in collaboration with Professor Andrew Hill from the University of Melbourne’s Bio21 Institute and Department of Biochemistry and Molecular Biology showed that malaria parasites are able to send out messages to communicate with other malaria parasites in the body. The study was published today in the journal Cell.

Professor Cowman said the researchers were shocked to discover that malaria parasites work in unison to enhance ‘activation’ into sexually mature forms that can be picked up by mosquitoes, which are the carriers of this deadly disease.

“When Neta showed me the data, I was absolutely amazed, I couldn’t believe it,” Professor Cowman said. “We repeated the experiments many times in many different ways before I really started to believe that these parasites were signalling to each other and communicating. But we came to appreciate why the malaria parasite really needs this mechanism — it needs to know how many other parasites are in the human to sense when is the right time to activate into sexual forms that give it the best chance of being transmitted back to the mosquito.”

Malaria kills about 700,000 people a year, mostly children aged under five and pregnant women. Every year, hundreds of millions of people are infected with the malaria parasite,Plasmodium, which is transmitted through mosquito bites. It is estimated that half the world’s population is at risk of contracting malaria, with the disease being concentrated in tropical and subtropical regions including many of Australia’s near neighbours.

Dr Regev-Rudzki said the malaria parasites inside red blood cells communicate by sending packages of DNA to each other during the blood stage of infection. “We showed that the parasites inside infected red blood cells can send little packets of information from one parasite to another, particularly in response to stress,” she said.

The communication network is a social behaviour that has evolved to signal when the parasites should complete their lifecycle and be transmitted back to a mosquito, Dr Regev-Rudzki said. “Once they receive this information, they change their fate — the signals tell the parasites to become sexual forms, which are the forms of the malaria parasite that can live and replicate in the mosquito, ensuring the parasites survives and is transmitted to another human.”

Professor Cowman said he hopes to see the discovery pave the way to new antimalarial drugs or vaccines for preventing malaria. “This discovery has fundamentally changed our view of the malaria parasite and is a big step in understanding how the malaria parasite survives and is transmitted,” he said. “The next step is to identify the molecules involved in this signalling process, and ways that we could block these communication networks to block the transmission of malaria from the human to the mosquito. That would be the ultimate goal.”

This project was supported by the National Health and Medical Research Council of Australia, Howard Hughes Medical Institute and the Victorian Government.

Journal Reference:

  1. Neta Regev-Rudzki, Danny W. Wilson, Teresa G. Carvalho, Xavier Sisquella, Bradley M. Coleman, Melanie Rug, Dejan Bursac, Fiona Angrisano, Michelle Gee, Andrew F. Hill, Jake Baum, Alan F. Cowman. Cell-Cell Communication between Malaria-Infected Red Blood Cells via Exosome-like VesiclesCell, 2013; DOI:10.1016/j.cell.2013.04.029