Tag Archives: Short chain fatty acids

Lost Faecalibacteria in IBD and IL-10 Influences Inflammasomes

Lab mouse
Mice deficient in IL-10 have over active inflammasomes, which cause colitis.
This week on TIBDI: A new review is published on the gut microbiome, IBD patients have less butyrate-producing bacteria, and IL-10 deficient mice are inflamed by inflammasomes.

Healthy Gut Microbiome in the Spotlight

The state of the intestinal microbiome, in essence the microbiota genome, is proving to be an important factor during disease development and progression. However before in depth studies are done to define disease-related microbiome profiles, it’s essential to also have an idea of what profiles define a healthy state. Dr. Emily B. Hollister of the Baylor College of Medicine and Texas Children’s Hospital reviewed the current literature. In general, the gut microbiome has approximately more than 10 million non-redundant genes, and a more diverse microbiome is healthier than less diverse one. Not everyone has the same types of populations of bacteria; most healthy microbiomes can be classified into three basic enterotypes. The influence of the microbiome extends to the immune system, cellular nutrition, cellular protection, metabolic processes and the functioning of the nervous system.

Lost Faecalibacteria in IBD

Many researchers are searching for the right probiotics to treat inflammatory bowel disease (IBD). To support this kind of search, simultaneous research investigating the microbiota in IBD patients as compared to healthy ones is also necessary. Wei Wang of Wuhan University recently published evidence that some major changes in the IBD microbiota are an increase in Bifidobacteria and Lactobacilli along with a loss of Faecalibacterium prausnitzii. The loss of F. prausnitzii was especially considerable in patients with active Crohn’s disease (CD). F. prausnitzii is known to produce butyrate, which is especially important for the formation of regulatory T cells in the colon. The author suggests that instead of focusing on common lactic acid producing probiotics in IBD, patients may be better served by looking at butyrate-producing probiotic species.

IL-10 Deficient Mice Inflamed by Inflammasomes

An interesting model of IBD is the interleukin (IL)-10 deficient mouse, which develops spontaneous colitis. Dr. J. Zhang of the Medical University of South Carolina found evidence that inflammasomes play a role in this model by promoting chronic intestinal inflammation. He found that loss of IL-10 increased the levels of NLRP3 and contributed to more inflammasome activity. This caused higher amounts of active IL-1β to be produced in gut tissues, which also led to increased colitogenic Th17. Blocking inflammsome activation successfully improved the colitis of the IL-10 deficient mice, suggesting that similar strategies could be useful in IBD.



Butyrate and Carbon Monoxide Are Promising for Inflammatory Bowel Disease.

Methyl butyrate 3D
Simple butyrate may be the key behind increased regulatory T cells in the colon.
This week on TIBDI: REG3γ shows its value during intestinal bacterial infection, a new method of carbon monoxide delivery shows anti-inflammatory promise and butyrate is the fuel that drives regulatory T cells in the colon.

Continue reading Butyrate and Carbon Monoxide Are Promising for Inflammatory Bowel Disease.

Thank Your Bacteria for Your Colon Regulatory T Cells

Valeric acid is a short chain fatty acid
Two key articles about intestinal flora and colon regulatory T cells (Tregs) were published. One showed that Clostridia strains in human flora lead to normal Treg induction. The other explains that it is mainly short chain fatty acid (SCFA) secretion by beneficial bacteria that induce the colon Tregs.

Regulatory T Cell Induction with Clostridia Strains

Many articles have been published that describe Treg induction after treatment with probiotic bacterial strains. Atarashi et al. puts a new twist on this concept with their latest publication in Nature. The difference is how they conducted their research. Using a clever, step-wise procedure with germ-free mice, they searched human feces specifically for strains that would induce Tregs in the colon. They found 17 Clostridium strains that could induce Tregs. Germ-free mice usually have few Tregs, but when the researchers colonized germ-fee mice with their mix, the number of Tregs was returned to normal levels. Supplementation with these strains also reduced signs of colitis.

Regulatory T Cell Induction with Short Chain Fatty Acids

In Science, Smith et al. showed that SCFA are one of the most important bacterial components that control colon Treg populations. They noted that germ-free mice had lowered SCFA in the colon and considered that this was the reason that Treg levels in germ-free were reduced. Replacing SCFA restored Treg levels in germ-free mice, and it even increased Treg in mice with normal intestinal flora. SCFA treatment also helped prevent colitis. Their experiments indicated that this was regulated via the SCFA receptor, GPR43, and only colonic Tregs expressed high amounts of it.

Do you think that SCFA are the only way that intestinal bacteria control Treg populiations? Please feel free to share your thoughts about these new findings.


Atarashi, K., Tanoue, T., Oshima, K., Suda, W., Nagano, Y., Nishikawa, H., et al. (2013). Treg induction by a rationally selected mixture ofClostridia strains from the human microbiota. Nature, 1–7. doi:10.1038/nature12331

Smith, P. M., Howitt, M. R., Panikov, N., Michaud, M., Gallini, C. A., Bohlooly-Y, M., et al. (2013). The Microbial Metabolites, Short-Chain Fatty Acids, Regulate Colonic Treg Cell Homeostasis. Science. doi:10.1126/science.1241165