Gut bacteria and Immune response

It appears that not only does our gut bacteria impact obesity, but also our immune system.  Interesting that obesity is associated with diabetes, which can be an autoimmune disease.  Lots of causation vs. correlation stuff to figure out.

From World Economic Forum;

Unhealthy gut bacteria can make vaccines less effective

Scientists have started examining the interactions between gut bacteria and responses to vaccines. A recent review article concluded that the composition of your gut microbiome can influence whether a vaccine has an effect in your body.

Unhealthy gut microbiome composition (or “dysbiosis”) can lead to inflammation. And that means more bacterial cells pass through the damaged lining of the gut, which stimulates further immune system responses. This is called “leaky gut.” Vaccines may not be as effective because the immune system is already busy dealing with these bacterial cells “leaking” through the gut.

On the other hand, having a diverse and “healthy” gut microbiome, and thus no gut inflammation and “leakiness,” might allow a person’s immune system to focus on responding to the vaccine effectively.

Recent research has also found that the effectiveness of the seasonal flu shot could be enhanced by intestinal bacteria. The immune system detects specific proteins from the bacteria, and this detection seems to increase the immune system’s response to the flu vaccine. Then your body has an easier time mounting an immune response if you are exposed to the real flu virus.

The first article referenced above is summarized as:

Studies of the relationship between the microbiome and the development and function of the immune system are demonstrating novel concepts that could significantly alter the way we treat disease and promote wellness. Several diseases, including inflammatory bowel disease, allergy/asthma, and diabetes, are associated with changes in composition of the microbiome. Recent findings suggest novel complex mechanisms by which the microbiome impacts immune cell development and differentiation. A major implication of these findings is that the composition of microbiome may ultimately affect vaccine efficacy. We explore here the potential role of the microbiome in vaccine responses in the context of our growing understanding of the relationship between the gastrointestinal microbiota, resident immune cell populations, and systemic immunity.

The research about the flu vaccine was not just associative, but identified a specific protein:

The first signs that TLR5 might regulate influenza vaccine responses emerged from a 2011 Nature Immunology study, in which Pulendran and his colleagues used a systems biology approach to observe how the immune systems of healthy adults reacted to the flu shot. The researchers found that TLR5 levels within three days of receiving the vaccine were strongly correlated to the strength of the antibody response against the virus. Why a protein that controls immune reactions to bacteria might influence antibodies against a viral vaccine was unclear; it was this question that led the researchers to perform further tests.

For the present study, Pulendran’s team inoculated a variety of mouse strains with trivalent inactivated influenza vaccine (TIV), one of two commonly used versions of the seasonal flu shot used on people. The researchers found that knockout mice lacking the TLR5 protein had significantly lower levels of antibodies after receiving the vaccine than wild-type mice. Because TIV does not interact directly with TLR5, the authors turned to the microbiome in search of clues to how the vaccine was affecting the innate immune system.

Experiments with germ-free mice and animals treated with antibiotics to deplete their microbes revealed similar responses to TIV: compared to normal mice, both groups of experimental animals showed weaker protective responses to the flu vaccine. Allowing gut microbes to colonize germ-free mice before the animals were inoculated restored a robust antibody response. To ensure that the lack of microbes did not cause inherent defects in immunity, the authors co-injected flagellin with TIV in antibiotic-treated or germ-free mice. They observed the same restorative effect on antibodies in each case.



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