Effect of cigarette smoke extract on the intestinal microenvironment of ulcerative colitis tissue

• Published in: JGH open 2020-12, Vol.4 (6), p.1191-1198
• Main Authors: Cannon, Aoife, Clarke, Niamh, MacCarthy, Finbar, Dunne, Cara, Kevans, David, Mahmud, Nasir, Lysaght, Joanne, O'Sullivan, Jacintha
• Format: Article
• Language: English
• Subjects: Age; Biopsy; Chemokines; cigarette smoke extract; Cigarettes; Inflammatory bowel disease; inflammatory proteins; Lymphocytes; Original; Proteins; Recruitment; Smoking; Software; T lymphocytes; Tumor necrosis factor-TNF
• ISSN: 2397-9070; 2397-9070
• DOI: 10.1002/jgh3.12422

Background and Aim Ulcerative colitis (UC) is an autoimmune disease characterized by inflammation in the gastrointestinal tract. The severity of UC is higher in nonsmokers than smokers; however, the biological mechanisms controlling this effect remain unknown. The aim of this study was to examine the effect of cigarette smoke extract (CSE) on inflamed and noninflamed colonic tissue from UC patients and to determine if inflammatory mediators, transcription factors, and T cell phenotypes are altered by CSE. Methods Blood and colonic biopsies were obtained from UC patients undergoing endoscopy. Biopsies were cultured in the presence or absence of CSE. Multiplex enzyme‐linked immunosorbent assay (ELISA) measured secreted levels of inflammatory mediators. Nuclear factor kappa‐light‐chain‐enhancer of activated B cells (NF‐κB) and Hypoxia‐inducible factor 1‐alpha (HIF‐1α) expression were measured by DNA‐binding ELISA. T cell phenotypes were assessed by flow cytometry in matched blood and biopsies. Results Secreted levels of interleukin 2 (IL‐2), interleukin 6 (IL‐6), tumor necrosis factor ‐ alpha (TNF‐α), chemokine (C‐C motif) ligand 2 (CCL2), and interleukin 10 (IL‐10) were significantly (all P