BUGS AND WORMS AND OTHER GREAT STUFF
A great article appeared last week on Gut Microbiota for Health,[i] on the overlooked mycobiome in digestive diseases. I’ve written about this topic several times before and am always very happy to see new research focused on the topic.
The authors of the paper[ii] point out that while the gut bacteria greatly outnumber fungi, this in no way diminishes fungi’s effects on the host. Cell size too, for example, must be taken into account – and many fungi cells are 100X bigger in volume than many bacteria. They produce, therefore, much larger amounts of byproducts which, even in low concentrates, may have profound impact. And, like bacteria, fungi “talk” to the immune system both locally (in the gut) and remotely (in the body as a whole).
Factors that influence the make-up of the mycobiome include diet, because foods like cheese, vegetables, etc. have fungi in and on them. The host interacts with all the microbiota it houses: for example, things like bile acids and so forth, can alter the mycobiome make-up. Finally, the other organisms of the gut influence the composition of the mycobiome. In fact, the bacteria are not alone in their influence: archeae, viruses (bacteriophages), and so forth likely play a role in determining mycobiome composition, although very little research has been done on this to date.
Some research points to fungi having a role in metabolic syndrome as well as cancer but…we are nowhere near having enough information on this to determine true relevance yet, let alone, mechanisms of action. Evidence is mounting for connections between fungi and other diseases ranging from autism to spondylitis to schizophrenia. And it looks very likely that the mycobiome is involved in the development of inflammatory bowel diseases, as I’ve written about before: “…a role of the mycobiota in disease, notably in IBD, is indicated by both descriptive data in humans and mechanistic data in mice.” There are distinct differences between those with IBD and healthy controls, confirmed by two independent studies.
In a mouse model, fungi have been shown to aggravate the severity of inflammation in IBD. This research supports the idea that the fungi work with the bacteria in such a way as to worsen IBD symptoms. In fact, another study in humans (which I described back in 2017) showed that the fungi, C. tropicalis, and the bacteria E. coli and S. marcescens, work together to form a biofilm (kind of a slimy mass that protects the organisms inside – think about the plaque on your teeth) that evokes an inflammatory immune response.[iii]
A 2018 study was conducted in Saudi Arabia on 15 children with Crohn’s disease.[iv] Their mycobiomes were compared to 20 healthy controls to see if they could accurately predict which children were sick or healthy. They found that Saccharomyces cerevisiae and S. bayanus were at significantly higher levels in the children with IBD, while overall diversity of the mycobiome was lower…and indeed, they absolutely could use these levels to correctly predict if the sample came from a child with IBD or a healthy child.
I sincerely hope I have more frequent opportunities to write about research into our commensal organisms other than our bacteria. Each element of our internal ecosystems probably plays an equally important role in determining our health status. The bacteria though are best known and most numerous, so they get all the press (and money). I have high hopes though that this is all going to change in the very near future.
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[i] https://www.gutmicrobiotaforhealth.com/en/the-gut-mycobiome-overlooked-in-digestive-diseases/
[ii] Richard, ML and Sokol, H. The gut mycobiota: insights into analysis, environmental interactions and role in gastrointestinal diseases. Nature Reviews. 2019.
[iii] https://www.gutmicrobiotaforhealth.com/en/new-review-explores-targeting-gut-bacteria-fungi-interactions-may-help-manage-chronic-intestinal-inflammation/
[iv] El Mouzan, M, et. al. Fungal dysbiosis predicts the diagnosis of pediatric Crohn’s disease. World Journal of Gastroenterology. 2018:24(39):4510-4516. doi: 10.3748/wjg.v24.i39.4510.