Faecalibacterium prausnitzii Supernatant Ameliorates DSS-induced Colitis in Mice via Regulating Monocytes and Macrophages / 胃肠病学

ABSTRACT

Background:The abundance of Faecalibacterium prausnitzii (Fp) is reduced in patients with inflammatory bowel disease (IBD).Previous studies demonstrated that the supernatant of Fp exerts an obvious anti-inflammatory effect in experimental colitis.Aims:To investigate the effect of Fp supernatant on monocytes/macrophages and colonic inflammation in dextran sulfate sodium (DSS)-induced colitis in mice.Methods:Thirty male C57BL/6J mice were randomly divided into control group,colitis group and Fp treatment group.Acute colitis was induced by drinking 4.5％ DSS in distilled water for seven days in colitis and Fp treatment groups.Mice in Fp treatment group were also given gastric infusion of Fp supernatant during the process of colitis induction.Weight loss,defecation and histopathological damage of colon tissue were observed.The percentages of monocytes and macrophages of different phenotypes in spleen and colonic lamina propria,as well as the serum levels of a series of inflammatory cytokines were detected by flow cytometry.Results:Compared with colitis group,Fp treatment showed an ameliorating effect on weight loss,shortening of colon length and histopathological damage (P ＜ 0.05).The percentages of total amount of monocytes and proinflammatory monocytes in spleen and colonic lamina propria,and the percentage of M1 macrophages in colonic lamina propria in Fp treatment group were significantly lower than those in colitis group;the percentage of M2 macrophages in colonic lamina propria in Fp treatment group was significantly higher than that in colitis group (P all ＜ 0.05).The serum levels of interleukin (IL)-10 and IL-4 in Fp treatment group were significantly higher than those in colitis group,and the levels of IL-6,interferon (IFN)-γ and chemokine CCL2 were significantly lower than those in colitis group (P all ＜ 0.05).Conclusions:Fp supernatant may exert anti-inflammatory effect in experimental colitis in mice via reducing proinflammatory monocytes,inducing M2 polarization of macrophages in inflamed colon,promoting secretion of anti-inflammatory cytokines,and inhibiting secretion of proinflammatory cytokines and chemokines.