Dismicrobism in inflammatory bowel disease and colorectal cancer: Changes in response of colocytes

Figure 1 One hypothesis on the initiation of the inflammatory process in inflammatory bowel disease bases on an abnormal Th1 response mediated by the secretion of interferon gamma and tumor necrosis factor-α while the chronic inflammation is supported by interleukin-5 and interleukin-13 secreted by Th2 cells. IFN: Interferon; TNF: Tumor necrosis factor; IL: Interleukin; IBD: Inflammatory bowel disease.

Figure 2 Eubiosis and dysbiosis exert different biochemical effects in the context of colocytes pathophysiology. IBD: Inflammatory bowel disease.

Figure 3 At eubiosis stage, the intestinal epithelium hosts a rich and equilibrated microbiota that promotes the barrier function. Microbial dysbiosis favors the production of genotoxins and metabolites associated with carcinogenesis. Moreover dysbiosis induces dysregulation of immune responses that cause inflammation promotion of carcinogenesis. SCFA: Small-chain fatty acids; E. coli: Escherichia coli.