Jung H C, Eckmann L, Yang S K, Panja A, Fierer J, Morzycka-Wroblewska E, Kagnoff M F
Department of Medicine, University of California, San Diego, La Jolla 92093-0623.
J Clin Invest. 1995 Jan;95(1):55-65. doi: 10.1172/JCI117676.
Pathogenic bacteria that penetrate the intestinal epithelial barrier stimulate an inflammatory response in the adjacent intestinal mucosa. The present studies asked whether colon epithelial cells can provide signals that are important for the initiation and amplification of an acute mucosal inflammatory response. Infection of monolayers of human colon epithelial cell lines (T84, HT29, Caco-2) with invasive strains of bacteria (Salmonella dublin, Shigella dysenteriae, Yersinia enterocolitica, Listeria monocytogenes, enteroinvasive Escherichia coli) resulted in the coordinate expression and upregulation of a specific array of four proinflammatory cytokines, IL-8, monocyte chemotactic protein-1, GM-CSF, and TNF alpha, as assessed by mRNA levels and cytokine secretion. Expression of the same cytokines was upregulated after TNF alpha or IL-1 stimulation of these cells. In contrast, cytokine gene expression was not altered after infection of colon epithelial cells with noninvasive bacteria or the noninvasive protozoan parasite, G. lamblia. Notably, none of the cell lines expressed mRNA for IL-2, IL-4, IL-5, IL-6, IL-12p40, IFN-gamma, or significant levels of IL-1 or IL-10 in response to the identical stimuli. The coordinate expression of IL-8, MCP-1, GM-CSF and TNF alpha appears to be a general property of human colon epithelial cells since an identical array of cytokines, as well as IL-6, also was expressed by freshly isolated human colon epithelial cells. Since the cytokines expressed in response to bacterial invasion or other proinflammatory agonists have a well documented role in chemotaxis and activation of inflammatory cells, colon epithelial cells appear to be programmed to provide a set of signals for the activation of the mucosal inflammatory response in the earliest phases after microbial invasion.
穿透肠道上皮屏障的病原菌会刺激相邻肠道黏膜发生炎症反应。目前的研究探讨了结肠上皮细胞是否能提供对急性黏膜炎症反应的启动和放大至关重要的信号。用人结肠上皮细胞系(T84、HT29、Caco-2)单层培养物感染侵袭性细菌菌株(都柏林沙门氏菌、痢疾志贺氏菌、小肠结肠炎耶尔森氏菌、单核细胞增生李斯特菌、肠侵袭性大肠杆菌),通过mRNA水平和细胞因子分泌评估,结果导致四种促炎细胞因子(IL-8、单核细胞趋化蛋白-1、GM-CSF和TNFα)的特定组合协同表达并上调。这些细胞经TNFα或IL-1刺激后,相同细胞因子的表达也会上调。相比之下,用非侵袭性细菌或非侵袭性原生动物寄生虫蓝氏贾第鞭毛虫感染结肠上皮细胞后,细胞因子基因表达未发生改变。值得注意的是,在相同刺激下,没有一个细胞系表达IL-2、IL-4、IL-5、IL-6、IL-12p40、IFN-γ的mRNA,或显著水平的IL-1或IL-10。IL-8、MCP-1、GM-CSF和TNFα的协同表达似乎是人类结肠上皮细胞的一个普遍特性,因为新鲜分离的人类结肠上皮细胞也表达相同的细胞因子组合以及IL-6。由于响应细菌侵袭或其他促炎激动剂而表达的细胞因子在炎症细胞的趋化作用和激活中具有充分记录的作用,结肠上皮细胞似乎被设定为在微生物侵袭后的最早阶段为黏膜炎症反应的激活提供一组信号。