Reimund J M, Wittersheim C, Dumont S, Muller C D, Baumann R, Poindron P, Duclos B
Service d'Hépatogastroentérologie et d'Assistance Nutritive, CHRU Hautepierre, Strasbourg, France.
J Clin Immunol. 1996 May;16(3):144-50. doi: 10.1007/BF01540912.
Chronic inflammation in inflammatory bowel disease (IBD; Crohn's disease and ulcerative colitis) may be attributed partly to increased secretion of inflammatory cytokines. The aim of this study was to investigate simultaneously the spontaneous release patterns of tumor necrosis factor-alpha (TNF-alpha), interleukin-1-beta (IL-1 beta), and interleukin-6 (IL-6) by organ cultures of inflamed mucosa from IBD patients. Organ cultures of involved IBD mucosa spontaneously produced increased amounts of TNF-alpha, IL-1 beta, and IL-6 compared to normal mucosa. The patterns of cytokine release between Crohn's disease and ulcerative colitis organ cultures were not significantly different. Increased inflammatory cytokine production by lamina propria mononuclear cells (LPMCs) and mucosa treated with EDTA suggests that these cytokines originate mainly from LPMCs. These results confirm the role of inflammatory cytokines in IBD and shed a new light on the role of TNF-alpha in IBD.
炎症性肠病（IBD，包括克罗恩病和溃疡性结肠炎）中的慢性炎症可能部分归因于炎性细胞因子分泌增加。本研究的目的是同时研究IBD患者炎症黏膜的器官培养物中肿瘤坏死因子-α（TNF-α）、白细胞介素-1-β（IL-1β）和白细胞介素-6（IL-6）的自发释放模式。与正常黏膜相比，受累IBD黏膜的器官培养物自发产生了更多的TNF-α、IL-1β和IL-6。克罗恩病和溃疡性结肠炎器官培养物之间的细胞因子释放模式没有显著差异。固有层单核细胞（LPMC）和用乙二胺四乙酸（EDTA）处理的黏膜产生的炎性细胞因子增加，表明这些细胞因子主要来源于LPMC。这些结果证实了炎性细胞因子在IBD中的作用，并为TNF-α在IBD中的作用提供了新的线索。
