PMC:7572937 / 8325-9414 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7572937","sourcedb":"PMC","sourceid":"7572937","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7572937","text":"a Neutrophils migrate into the inflamed GI tract toward various chemoattractants. In the case of Toxoplasma gondii and bacterial infection, neutrophils migrate to the gut lumen in an FPR1-dependent manner to regulate bacterial containment and to separate luminal contents from the epithelium. Neutrophils activated by FPR1 remove microenvironmental oxygen by NOX2-mediated ROS generation, resulting in local enrichment of an anaerobic bacterial consortium. In particular, Akkermansia muciniphila facilitates epithelial wound healing through an epithelial NOX1-dependent mechanism. Monocytes, which facilitate epithelial remodeling during wound closure, migrate into the inflamed site via the CCL20-CCR6 axis. FPR2 expression is related to the expression of CCR6 in monocytes. b M cells and DCs in Peyer’s patches recognize LL-37 via FPR2, promoting DC activation with increased phagocytosis, expression of CD40, and production of IL-6 and IL-12. Follicular DCs express CXCL13 and B cell-activating factor, supporting germinal center B cell activation in Peyer’s patches via FPR2 signaling.","tracks":[]}