Sphingolipids as Mediators in the Crosstalk between Microbiota and Intestinal Cells: Implications for Inflammatory Bowel Disease

Figure 2

Known effects of pathogenic bacteria, microbiota members, and probiotics on SL signaling in IBD. Probiotics increase SMase activity and diminish intestinal inflammation reducing mucosal damage in both humans and a mouse model. Bacteroides fragilis, a known microbiota member, induces inflammation by stimulating epithelial production of IDENs containing high levels of S1P and mediating Th17 recruitment. Conversely, the pathogen Shigella flexneri can avoid the inflammatory response by decreasing S1P levels, downregulating SK2 expression and increasing SPL and S1PPs expression. SM: sphingomyelin, LPCs: lysophosphatidylcholines, GPCs: glycerophosphatidylcholines, IL-6: interleukin-6, ILPMC: intestinal lamina propria mononuclear cells, IDENs: intestinal derived exosome like nanoparticles, S1P: sphingosine 1 phosphate, SK2: sphingosine 1 phosphate kinase 2, SPL: sphingosine 1 phosphate lyase, and S1PPs: sphingosine 1 phosphate phosphatases.