Metabolic syndrome attenuates ulcerative colitis: Correlation with interleukin-10 and galectin-3 expression

• Published in: World journal of gastroenterology : WJG Vol. 25; no. 43; pp. 6465 - 6482
• Main Authors: Jovanovic, Marina, Markovic, Bojana Simovic, Gajovic, Nevena, Jurisevic, Milena, Djukic, Aleksandar, Jovanovic, Ivan, Arsenijevic, Nebojsa, Lukic, Aleksandra, Zdravkovic, Natasa
• Format: Journal Article
• Language: English
• Published: United States Baishideng Publishing Group Inc 21.11.2019
• Subjects: Adult; Aged; Aged, 80 and over; Case-Control Studies; Colitis, Ulcerative - blood; Colitis, Ulcerative - complications; Colitis, Ulcerative - immunology; Colitis, Ulcerative - pathology; Colon - immunology; Colon - pathology; Cytokines - blood; Feces - chemistry; Female; Galectin 3 - blood; Humans; Lymphocytes - metabolism; Male; Metabolic Syndrome - blood; Metabolic Syndrome - complications; Metabolic Syndrome - immunology; Middle Aged; Observational Study; Young Adult; Systemic immune response; Inflammation; Galectin-3; Interleukin-10; Metabolic syndrome; Ulcerative colitis
• DOI: 10.3748/wjg.v25.i43.6465
• ISSN: 1007-9327; 2219-2840

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. To test the influence of the MetS on the severity of UC and the local and systemic immune status. Eighty nine patients with histologically confirmed UC were divided in two groups, according to ATP III criteria: Group without MetS (no MetS) and group with MetS. 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 factor α (TNF-α), interleukin-6 (IL-6), and interleukin-17 (IL-17) in the sera as well as Gal-3 over TNF-α and 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. 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.