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Metabolic syndrome attenuates ulcerative colitis: Correlation with interleukin-10 and galectin-3 expression 被引量:6
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作者 Marina Jovanovic Bojana Simovic Markovic +6 位作者 Nevena Gajovic Milena Jurisevic Aleksandar Djukic Ivan Jovanovic Nebojsa Arsenijevic Aleksandra Lukic natasa zdravkovic 《World Journal of Gastroenterology》 SCIE CAS 2019年第43期6465-6482,共18页
BACKGROUND Ulcerative colitis(UC)is a chronic disease characterized by inflammation of intestinal epithelium,primarily of the colon.An increasing prevalence of metabolic syndrome(MetS)in patients with UC has been docu... BACKGROUND Ulcerative colitis(UC)is a chronic disease characterized by inflammation of intestinal epithelium,primarily of the colon.An increasing prevalence of metabolic syndrome(MetS)in patients with UC has been documented recently.Still,there is no evidence that MetS alters the course of the UC.AIM To test the influence of the MetS on the severity of UC and the local and systemic immune status.METHODS Eighty nine patients with de novo histologically confirmed UC were divided in two groups,according to ATP III criteria:Group without MetS(no MetS)and group with MetS.RESULTS Clinically and histologically milder disease with higher serum level of immunosuppressive cytokine interleukin-10(IL-10)and fecal content of Galectin-3(Gal-3)was observed in subjects with UC and MetS,compared to subjects suffering from UC only.This was accompanied with predomination of IL-10 over pro-inflammatory cytokines tumor necrosis factorα(TNF-α),interleukin-6(IL-6),and interleukin-17(IL-17)in the sera as well as Gal-3 over TNF-αand IL-17 in feces of UC patients with MetS.Further,the patients with both conditions(UC and MetS)had higher percentage of IL-10 producing and Gal-3 expressing innate and acquired immune cells in lamina propria.CONCLUSION Local dominance of Gal-3 and IL-10 over pro-inflammatory mediators in patients with MetS may present a mechanism for limiting the inflammatory process and subsequent tissue damage in UC. 展开更多
关键词 ULCERATIVE COLITIS Metabolic syndrome GALECTIN-3 Inflammation INTERLEUKIN-10 Systemic immune response
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