Chu Hong-Qian, Li Jun, Huang Hong-Peng, Hao Wei-Dong, Duan Li-Ping, Wei Xue-Tao
Department of Toxicology, School of Public Health, Peking University, Beijing, PR China; Beijing Key Laboratory of Toxicological Research and Risk Assessment for Food Safety, Beijing, PR China.
Department of Gastroenterology, Peking University Third Hospital, Beijing, PR China.
Dig Liver Dis. 2016 Feb;48(2):162-71. doi: 10.1016/j.dld.2015.09.002. Epub 2015 Sep 25.
Mast cells in the gut play an important role in the innate and adaptive immune responses that are relevant to human inflammatory bowel disease. However, the contribution of mast cells to the development of inflammatory bowel disease is not well understood. This study aimed to determine the role of mast cells in oxazolone-induced colitis and to explore whether the mast cell membrane stabiliser tranilast could ameliorate colonic inflammation.
Wild-type rats and mast cell-deficient rats were sensitised and challenged with oxazolone, then treated with tranilast after challenge. Controls were treated with saline.
Mast cell-deficient rats presented a weak response to oxazolone, while wild-type rats showed severe ulcerative colitis after stimulation with oxazolone. The mast cell-deficient rats model had a significantly lower disease activity index score than wild-type rats model (1.8±1.64 vs. 8.3±0.58 respectively; P<0.01). Tranilast could reduce the secretion of cytokines, immunoglobulins and myeloperoxidase activity in tranilast treatment groups compared with the model group. The number of mast cells in the wild-type model was higher than in the other groups. There was no significant change in mast cell-deficient rats.
Mast cells play an important role in oxazolone-induced colitis. The mast cell membrane stabiliser tranilast can ameliorate oxazolone-induced colitis via a mast cell-dependent pathway.
肠道中的肥大细胞在与人类炎症性肠病相关的先天性和适应性免疫反应中发挥重要作用。然而,肥大细胞对炎症性肠病发展的贡献尚未得到充分了解。本研究旨在确定肥大细胞在恶唑酮诱导的结肠炎中的作用,并探讨肥大细胞膜稳定剂曲尼司特是否可以改善结肠炎症。
野生型大鼠和肥大细胞缺陷型大鼠用恶唑酮致敏并激发,激发后用曲尼司特治疗。对照组用生理盐水治疗。
肥大细胞缺陷型大鼠对恶唑酮反应较弱,而野生型大鼠在恶唑酮刺激后出现严重的溃疡性结肠炎。肥大细胞缺陷型大鼠模型的疾病活动指数评分显著低于野生型大鼠模型(分别为1.8±1.64和8.3±0.58;P<0.01)。与模型组相比,曲尼司特治疗组可降低细胞因子、免疫球蛋白的分泌以及髓过氧化物酶活性。野生型模型中的肥大细胞数量高于其他组。肥大细胞缺陷型大鼠无显著变化。
肥大细胞在恶唑酮诱导的结肠炎中起重要作用。肥大细胞膜稳定剂曲尼司特可通过肥大细胞依赖性途径改善恶唑酮诱导的结肠炎。