Abstract
The beneficial role of gut microbiota in intestinal diseases has been highlighted recently. Bacteroides fragilis found in the human gastrointestinal tract is a well-studied example of a beneficial bacterium that protects against intestinal inflammation. Polysaccharide A (PSA) from B. fragilis induces the production of interleukin (IL)-10 from immune cells via Toll-like receptor 2 (TLR2) signaling in animal colitis models. The direct effect of PSA on human colorectal cancer (CRC) cells has not been studied. Here, we report the effect of PSA from B. fragilis on CRC pathogenesis in SW620 and HT29 CRC cells and the molecular signaling underlying these effects. We demonstrated that PSA induced the production of the pro-inflammatory cytokine, IL-8, but not IL-10, in CRC cells. PSA inhibited CRC cell proliferation by controlling the cell cycle and impaired CRC cell migration and invasion by suppressing epithelial mesenchymal transition. Moreover, as in the case of other animal intestinal diseases, the protective role of PSA against CRC pathogenesis was also mediated by TLR2. Our results reveal that PSA from B. fragilis plays a protective role against CRC via TLR2 signaling.
Highlights
Commensal bacteria can regulate the colonic epithelial barrier, which is the first line of defense that protects the body from the gastrointestinal environment
The results demonstrated that the colorectal cancer (CRC) cells expressed the cytokines CXCL8, IL1B, IL10, and transforming growth factor beta 1 (TGFB1) (Figure 1A)
Polysaccharide A (PSA) could not suppress the migration (Figure 5E) and invasion (Figure 5F) of shRNA targeting TLR2 (shTLR2) cells as it did in shCtrl cells. These findings demonstrated that the effects of B. fragilis PSA on the proliferation, migration, and invasion of CRC cells are mediated by Toll-like receptor 2 (TLR2) signaling
Summary
Commensal bacteria can regulate the colonic epithelial barrier, which is the first line of defense that protects the body from the gastrointestinal environment. The commensal bacteria might interact with and modulate the intracellular mechanism of colonic epithelial cells. Probiotic bacteria such as Bifidobacterium, which reside in the gastrointestinal tract, were shown to reduce tumor volume in rats, indicating a potential role of the gut microbiota in tumor suppression (Singh et al, 1997). There are trillions of commensal microorganisms residing in the gastrointestinal tract that play an important role in regulating the immune system of the gut.
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