Dysbiosis is a real kick in the guts.

In your body, an intact gut lining acts as a gatekeeper, allowing vital nutrients and substances to pass through while stopping large molecules, toxins and pathogens from entering your bloodstream. Your immune system also plays a role, responding with inflammation if the lining in your gut is compromised.

How you feel, your mood, and your general health is affected by the quality of your gut lining. And it’s the trillions of bacteria setting up shop in our gut that carry out tasks to ensure that the gastrointestinal system stays in top condition. [1]

Your star micrboes include members of the Firmicutes group which make butyrate, a short-chain fatty acid that is the main energy source for the cells in your gut lining. Butyrate enables these cells to prevent the lining from becoming too porous, which would otherwise lead to an inflammatory response to the unwanted substances passing through.

Butyrate also reinforces the mucous layer in the gut lining. The mucus is a food source for a type of bacteria called Akkermansia muciniphila which in turn produces another short-chain fatty acid, acetate. Firmicutes then use acetate to make more butyrate which increases the production of mucin, a protein responsible for increasing the thickness and strength of your gut lining.

Without this coordinated teamwork, the gut lining becomes compromised and health issues can ensue.

NLRP6 inflammasome is a protein that plays a protective role in the immune system. Highly expressed in the intestine and liver, its role is to regulate inflammation and the composition of the microbiota.

Research by Richard Flavell et al [2] found that deficiencies in the NLRP6 inflammasome resulted in an imbalance (otherwise known as dysbiosis) in the gut microbiota of mice. The altered population of microbes led to inflammation of the colon, a condition known as colitis.

Interestingly, this colon-inflaming microbial population was transferred to wild-type mice (“normal mice”) who were co-living with the NLPR6 inflammasome mice. It also induced exacerbated inflammatory bowel disease (IBD) in both the NLPR6-deficient mice and the wild-type mice

How crazy a thought that a disease can be transmitted to healthy animals through a transmitted change in their gut microbiota? If it turns out this is also the case in humans, could transferable microbes be linked in some way to the recent rapid rise in obesity and other diseases?

The ‘disappearing microbiota’ hypothesis [3] suggests that ecological changes over the past 100 or so years have contributed to a shift in the types of organisms now found in the gut with a knock-on effect on disease risk.

This hypothesis, along with Flavell’s study, highlights that changes to the composition of our microbiome can have unwanted repercussions for our guts.

Bacteria are frequently portrayed as enemies. However, in the right context, such as their role in keeping your gut lining functioning optimally, bacteria can also be our heroes; a point worth remembering in this new age of antibiotic abundance and hyper cleanliness.

Brigid xx

References

[1] Harvard Health Publishing. (2016). Can Gut Bacteria Improve Your Health? Harvard Medical School.

[2] Elinav, Eran et al. “NLRP6 inflammasome regulates colonic microbial ecology and risk for colitis.” Cell vol. 145,5 (2011): 745-57. doi:10.1016/j.cell.2011.04.022

[3] Blaser, Martin J. Missing Microbes. HarperCollins Publishers, 2014.