Microbiome Dysbiosis and Oxygen

Apr 27 / Kristina Mitts
In the last blog post we talked about dysbiosis signatures vs. the signature of a healthy gut. I mentioned towards the end that we want our gut microbiome to be dominated by anaerobic microbes - that is to say - not tolerant of oxygen.



When the microbiome becomes dysbiotic it tends to contain more oxygen tolerant microbes. Well this blog post explains why that occurs and what you can do to prevent it. Thanks to research by Yael Litvak et al in Science Journal we now understand why it is that a dysbiotic microbiome tends to contain more oxygen tolerant microbes such as Staphylococcus, Streptococcus, Escherichia coli, Salmonella, Listeria and Shewanella.

These bacteria tend also to metabolize fermentation products to carbon dioxide when oxygen is present. Moreover, the epithelial lining becomes rich with oxygen rather than being hypoxic. In a normal healthy microbiome experiencing homeostasis the cells that line the intestinal tract metabolize oxygen quickly and efficiently; making the area hypoxic (free of oxygen). However, when they become inflamed or damaged they can no longer metabolize oxygen as efficiently.

See the above diagram. Blood vessels line the outside of the digestive tract in order to bring nutrients and oxygen to the cells. Oxygen and nutrients diffuse through to the epithelial cells which line your digestive tract. When dysbiosis occurs the lining becomes inflamed and the cells don’t metabolize oxygen as well. This means that oxygen diffuses further into the gut, promoting an environment that favours oxygen tolerant microbes.

In simplified terms the CELLS are not taking in the oxygen , but instead the oxygen diffuses through the epithelial lining.

The authors found that any condition that shifts the metabolism of colonocytes away from lipid oxidation causes an increase in the amount of oxygen emanating from the mucosal surface, thereby driving a shift in the microbial community from obligate to facultative anaerobes, a hallmark of dysbiosis in the colon. 

So what shifts metabolism towards lipid oxidation.. and furthermore epithelial hypoxia? The answer is butyrate. Butyrate actives PPAR-y signaling in epithelial cells to drive mitochondrial beta oxidation of fatty acids. This promotes more oxygen metabolism by the cells, upregulates tight junctions and promotes growth of anaerobic microbes.

Meanwhile, studies find that antibiotic mediated depletion of short chain fatty acids silences epithelial PPAR-y signalling and lowers T reg cells. The authors provide another beautiful diagram comparing healthy macrophage and healthy epithelial cell to unhealthy ones.

All of this makes me wonder how it is that Hyperbaric Oxygen is so beneficial in dysbiotic conditions such as Ulcerative Colitis and Crohns? Given that mitochondria are mentioned I imagine there may be some work around to do with mitochondrial signalling. Perhaps hypoxia inducible factor may somehow set off a chain of events wherein PPAR-y signalling and beta oxidation of fatty acids is turned on. Due to this question I've decided to interview Hyperbaric Oxygen technician and Antiaging Biologist Andrew Paterson.You can join us for the live or watch the replay here: 

https://www.wildbiome.ca/course/hyperbaric-oxygen-with-andrew-paterson?site_template_id=61d13d556bada43701395445



Reference:DOI: 10.1126/science.aat9076
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