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Friday, 26 January 2018


"The aim is to bring novel microbiome diagnostic systems to populations, then use food and probiotics to try and improve biomarkers of health," says study co-author Gregor Reid, a professor at Western University's Schulich School of Medicine & Dentistry and a scientist at Lawson Health Research Institute. However, the study cannot explain causality. As Prof. Reid explains, "It begs the question "if you can stay active and eat well, will you age better, or is healthy aging predicated by the bacteria in your gut?" Either way, there remains a strong and undeniable correlation between a healthy gut and healthy aging.

"The main conclusion is that if you are ridiculously healthy and 90 years old, your gut microbiota is not that different from a healthy 30-year-old in the same population." – Prof. Grg Gloor 

"Whether this is cause or effect is unknown," write the authors. However, Prof. Gloor explains, "This demonstrates that maintaining [the] diversity of your gut as you age is a biomarker of healthy aging, just like low-cholesterol is a biomarker of a healthy circulatory system." "By studying healthy people, we hope to know what we are striving for when people get sick," notes Prof. Reid.

The results of the study, the authors write, "[suggest] that resetting an elderly microbiota to that of a 30-year-old might help promote health."


At present, the Centers for Disease Control (CDC) estimate that 1 in 68 children will be diagnosed with an autism spectrum disorder. There is no known cause for autism. Autism encompasses a range of conditions and disorders, from mild to severe, so there is likely more than one cause, depending on the child. Research is ongoing in many labs to find as much information as possible. Whether there is a genetic link, an environmental cause, or an immune system factor, finding out about the biology behind autism remains a goal for many in the scientific community.

Recent research by scientists from the University of Massachusetts and MIT suggests that an infection during pregnancy could be connected to an increased risk of giving birth to a child who will develop autism. Knowing how this infection presents could help in the understanding of how autism behaviours in offspring develop and whether or not the infection changes the brains of babies in utero. There are two papers that were published recently, and both papers had the same two scientists as lead authors. They are Gloria Choi, who is an Assistant Professor of Brain and Cognitive Sciences at MIT and a member of the McGovern Institute for Brain Research and Jun Huh, a former assistant professor at UMass Medical School and currently a faculty member at Harvard Medical School. Together, they have published research that looked strains of bacteria in the gut of pregnant women.

The connection between gut bacteria and autism was investigated in a 2010 Danish study that found a correlation between certain viral infections during early pregnancy and a nearly three-fold increased risk of having a child with autism. Choi and Huh published research in 2016 on immune cells, known as Th17 cells and the molecule that activates them (the IL-17 molecule.) In mouse models it was found that inflammation in these cells causes a reaction in the developing brain receptors of a foetus in specific parts of the cortex. Their published work investigated further how “patches” of these receptors in the brains of babies in utero might be a factor in behavioural abnormalities common in autism, such as self-stimming behaviours, repetitive motions, and social difficulties.

One of the papers detailed the role of a protein expressed in the somatosensory cortex and autism behaviours. This is where the brain handles proprioception, the ability to know where one’s body is in the environmental space around it. Intraneurons in this region express a protein called parvalbumin, but in mice that were found to have irregularities in this area, due to inflammation, there were less of these intraneurons and areas of the somatosensory cortex were overexcited in the expression of this protein.

When the researchers were able to normalize the balance in this brain area, behavioral abnormalities in the mice were reversed. Inducing the overstimulation of these neurons resulting in behavioural abnormalities in normal mice. Being able to manipulate the process is key to finding a treatment.

Adapted from Brenda Kelley Kim who is a writer living in the Boston area with interest in cancer research, cardiology and neuroscience. 

Rare Microbes Make a Critical Contribution to the Environment.

New work published in Applied Environmental Microbiology suggests that bacteria present at very small levels in the environment actually make a vital contribution to the health and stability of that environment. This research concerns microbes that don’t usually account for more than a tenth of a percent of the bacteria in the whole population. "The work aims to provide a fundamental understanding of how biodiversity contributes to ecosystem functioning," said the corresponding author of the work, Kostas Konstantinidis, PhD.

In the environment at large, these are low levels, but in individual communities there may be hundreds of them, actually therefore, composing 20 to 30 percent of specific bacteria in an aquatic group.Termed the rare biosphere, these uncommon species were found to harbor large amounts of genes capable of allowing for organic pollutant degredation. The abilities conferred by those microbes may be helping the entire microbial population remain stable in the face of environmental pressures and alterations. The investigators, a team from Georgia Institute of Technology, Atlanta, wanted to test this idea, so they created mesocosms, or laboratory environments, made up of 20 liters of water. These reservoirs were then inoculated with water samples taken from a local freshwater source, Lake Lanier. An illustrative example of a mesocosm is shown in the video above.

Three common organic chemicals, not present in the samples they took from the lake, were then dribbled into the mesocosms. The scientists wanted ot ensure that the microbes had not be acclimated to the presence of those pollutants in order to reveal as much as possible about the microbes’ abilities. "Also, the important environmental pollutants are generally at low concentration in most natural environments, similar to the organic compounds used here--except during major events such as oil spills" said Konstantinidis, the Carlton S. Wilder Associate Professor in the School of Civil & Environmental Engineering at Georgia Tech.

The pollutants used included 2,4-dichlorophenoxyacetic acid (2,4-D), a common herbicide that is a known endocrine disrupter and may be a carcinogen, according to the International Agency for Research on Cancer. The other compounds were caffeine (1,3,7-trimethyluric acid) and 4-nitrophenol (4-NP), used in fungicide production and one byproduct of pesticide breakdown."We chose these compounds because their biodegradation pathways and the underlying genes are known, which facilitated tracking which microbial populations encoded the proteins for the biodegradation of these organic compounds," explained Konstantinidis. The researchers repeatedly assayed the bacterial levels in the mseocosms to find which ones grew more or grew less. "The results allowed us to rigorously test the hypothesis that low abundance species, as opposed to common species, provided the metabolic diversity that enabled the community to respond to the added compounds and the changing conditions," said Konstantinidis.

The goal of the work was to improve our predictions of how microbial communities might react to future disruptions from stuff like oil, pesticides, or climate change, said Konstantinidis. We may learn a lot more about how microbes contribute to the function and resilience of our ecosystem, and the possible consequences microbes face due to contaminant spills or climate change. In a Tedx talk, speaker Duccio Cavalieri, Ph.D. explains why maintaining diversity among microbes is to everyone’s benefit.

Sources: AAAS/Eurekalert!, American Society for Microbiology, Applied Environmental Microbiology 



Is it true that you are what you eat? Well, have some bacteria then and get happy. Actually it’s much more complex than that. New research from the University of Virginia School of Medicine (UVA) has shown that depressive symptoms and behaviours in mice were reversed when the mice were given food containing lactobacillus, which is a probiotic bacteria found in yogurt that is made with live cultures. The research was even able to uncover the specific process for how these probiotics impacted mood. Finding a link that makes such a close connection between the gut microbiome and mental health is a major step forward in learning more about depression and how it can be treated.

Depression isn’t just feeling sad for a while, it’s a very real neurobiological illness. Major depressive disorder affects approximately 14.8 million American adults, or about 6.7 percent of the U.S. population age 18 and older, in any given year. As many as one in 33 children and one in eight adolescents have clinical depression. Depression also puts those who suffer with it at a higher risk for heart attacks, even if they have no other cardiovascular risk factors. Since depression can seriously hinder things like a person’s ability to have a rewarding career and a stable family life, research into treatments and causes are crucial.

Lead researcher on the study at UVA, Alban Gaultier, stated, “The big hope for this kind of research is that we won’t need to bother with complex drugs and side-effects when we can just play with the microbiome. It would be magical just to change your diet, to change the bacteria you take, and fix your health – and your mood. It’s a huge problem and the treatments are not very good, because they come with huge side-effects.”

So what exactly is the “gut microbiome?” It’s the living bacteria inside the intestinal tract that is responsible for, among other things, keeping the body in balance. It’s a popular target of researchers looking into all kinds of illnesses. Connecting it to mental illness or other neurological conditions has been difficult. However, since the mouse model is used in research because of its similarity to humans, Galtier’s team looked at mice that were subjected to stress since stress can cause depression. Of course in mice, it was more about observing how they acted and looking for “depressive like behaviors” and “despair behavior” since there is obviously no other way to judge mood in animals.

When the gut microbiome composition was examined in the mice, both before and after a period of stress there was one major change that stood out. The bacteria lactobacillus was reduced in correlation to the onset of depressive behaviors in the mice. When the researchers added lactobacillus cultures back to the food of the depressed mice, the behaviors stopped and they began to behave as they had before the stress was induced.

The research at UVA took it a step further and also investigated how exactly this mechanism of lactobacillus fluctuation worked. Their study revealed that amounts of Lactobacillus in the gut will impact levels of a metabolite in the blood called kynurenine which is known to fuel depression. When lactobacillus went down, kynurenine went up and the despair behaviors of the mice began. The team hopes that they can translate these results in humans. Graduate student Ioana Marin, a researcher on the study said, “There has been some work in humans and quite a bit in animal models talking about how this metabolite, kynurenine, can influence behavior. It’s something produced with inflammation that we know is connected with depression. But the question still remains: How? How does this molecule affect the brain? What are the processes?” This are the begging questions scientist are looking answer for. 


Our guts are home to a complex community of more than 100 trillion microbial cells that play an important role in health and disease.
These gut-resident microbes, or gut microbiota - which with their genetic material are known as the gut microbiome - influence metabolism, nutrition, and immune function.
Scientists are discovering that disruption in the gut microbiota is linked to obesity, inflammatory bowel disease, and other gastrointestinal disorders. It has also been suggested that obesity’s effect on the gut microbiome may explain its strong link with type 2 diabetes. Others have likened the uniqueness of a person's gut microbiota to that of a "DNA fingerprint," raising potential privacy concerns for participants of human microbiome research projects.
In this particular study the cell called dendritic cells (DCs) that have evolved two distinctive - and what may appear to be opposite - roles in the human body, in that they can both promote and inhibit immune response. DCs help to activate the immune system in response to infection, but they are also involved in actively suppressing it in certain situations.They suppress immunity by triggering induced regulatory T cells (iTregs), a type of cell that controls the development of immune tolerance.
As immunity inhibitors in the gut, DCs help to train the immune system to treat gut microbiota as friend rather than foe. They do this by internalizing proteins from the microbiota and migrating to lymph nodes associated with the gut. As they travel to the lymph nodes, the DCs break down the internalized friendly bacteria proteins into smaller pieces that become similar to “identity badges” that they wear on their cell surfaces.
These identity badges are displayed with specific binding proteins that iTregs recognize, with the effect that the iTregs do not promote immune responses against proteins wearing the identity badges. Prof. Brocker says: "We believe that these iTregs are specific for the proteins produced by natural gut bacteria." The team explains that the migration to lymph cells by the DCs - particularly those whose cell surfaces display a protein called CD103+ - is an important part of keeping the immune system updated on the composition of the gut microbiota. However, what the researchers wanted to discover was how this tolerance mechanism might be switched off in an emergency. Their investigation led them to another molecule that DCs display on their cell surfaces - known as CD40 - that behaves in a similar way to an alarm button. When activated, CD40 binds to a partner molecule on the surface of another type of T cell effector T cells, which turns DCs from inhibitors of immune response to promoters. In tests on mice, the researchers showed that animals whose CD40 signalling was permanently switched on developed severe colitis, but no other symptoms.
They found that the affected dendritic cells still migrate to the lymph nodes from the gut lining, but when they get there they commit cell suicide (apoptosis) and thus deny the regulatory T cells the opportunity to sense the identity badges of the microbiota proteins that would normally protect them from immune attack. This results in a generalized immune response in which T lymphocytes travel to the gut lining and cause inflammation. The team found that giving the mice antibiotics that killed their gut microbiota also reduced the inflammation, and the animals survived. The researchers now want to find out whether particular regulatory T cells are programmed for specific gut bacteria, as this study might suggest.
Culled from Catherine paddock (PhD) write up

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