Objective Ulcerative colitis is a prevalent immunoinflammatory ***17/Treg cell imbalance and gut microbiota dysregulation are key factors in ulcerative colitis *** actin cytoskeleton contributes to regulating the prol...
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Objective Ulcerative colitis is a prevalent immunoinflammatory ***17/Treg cell imbalance and gut microbiota dysregulation are key factors in ulcerative colitis *** actin cytoskeleton contributes to regulating the proliferation,differentiation,and migration of Th17 and Treg ***63,a gene containing the WD repeat domain,participates in the structure and functional modulation of actin *** research indicates that WDR63 may serve as a regulator of cell migration and metastasis via actin polymerization *** article aims to explore the effect of Wdr63 deletion on Th17/Treg cells and ulcerative *** We constructed Wdr63-/-mice,induced colitis in mice using dextran sulfate sodium salt,collected colon tissue for histopathological staining,collected mesenteric lymph nodes for flow cytometry analysis,and collected healthy mouse feces for microbial diversity *** Compared with wild-type colitis mice,Wdr63-/-colitis mice had a more pronounced shortening of colonic tissue,higher scores on disease activity index and histological damage index,Treg cells decreased and Th17 cells increased in colonic tissue and mesenteric lymph nodes,a lower level of anti-inflammatory cytokine IL-10,and a higher level of pro-inflammatory cytokine *** addition,WDR63 has shown positive effects on maintaining intestinal microbiota *** maintains the balance of Bacteroidota and Firmicutes,promoting the formation of beneficial intestinal bacteria linked to immune *** Wdr63 deletion aggravates ulcerative colitis in mice,WDR63 inhibits colonic inflammation likely by regulating Th17/Treg balance and maintains intestinal microbiota homeostasis.
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