Coconnier M H, Bernet-Camard M F, Servin A L
Département de Microbiologie et Immunologie, UFR de Sciences Pharmaceutiques Paris XI, Châtenay-Malabry, France.
Differentiation. 1994 Nov;58(1):87-94. doi: 10.1046/j.1432-0436.1994.5810087.x.
In the human intestine, target cells of enteropathogens differentiate during cell migration along the crypt-villus axis. We have recently provided evidence that intestinal cell differentiation up-regulates intestinal cell infection by the noninvasive enterotoxigenic Escherichia coli [5, 23]. Several enterovirulent bacteria can penetrate intestinal epithelial cells, which are normally nonphagocytic. To document the role of intestinal epithelial cell differentiation in the pathogenesis of enteroinvasive bacteria, we examined here the intestinal cell-association and cell-entry of Yersinia pseudotuberculosis as a function of cell differentiation. For this purpose we used the colon carcinoma Caco-2 cell line in culture, which provides the most useful tool for the study of intestinal epithelial cell differentiation, because of its unique ability to spontaneously differentiate upon reaching confluence in normal culture condition. We report here that the thermoregulated inv and ail loci of Y. pseudotuberculosis have distinct roles in infection of Caco-2 cells. The ail locus initiates the cell-association and the inv locus initiates both the cell-association and the cell-entry processes. Moreover, we observed that: (i) both the bacterial cell-association (ail) and the bacterial cell-invasion (inv) occur at subconfluence when the Caco-2 cells are undifferentiated, and (ii) these processes are arrested when the differentiation commences. Since the integrin-beta 1 heterodimers are involved in cell-entry of Y. pseudotuberculosis in several mammalian cells, we further examined which beta 1 integrin promotes bacterial cell-entry in Caco-2 cells.(ABSTRACT TRUNCATED AT 250 WORDS)
在人类肠道中，肠道病原体的靶细胞在沿隐窝 - 绒毛轴的细胞迁移过程中发生分化。我们最近提供的证据表明，肠道细胞分化可上调非侵袭性产肠毒素大肠杆菌对肠道细胞的感染[5,23]。几种肠道致病细菌可穿透通常不具有吞噬作用的肠道上皮细胞。为了证明肠道上皮细胞分化在侵袭性细菌发病机制中的作用，我们在此研究了假结核耶尔森菌的肠道细胞黏附及细胞进入情况与细胞分化的关系。为此，我们使用了培养的结肠癌细胞系Caco - 2，由于其在正常培养条件下达到汇合时具有自发分化的独特能力，它为研究肠道上皮细胞分化提供了最有用的工具。我们在此报告，假结核耶尔森菌的温度调节型inv和ail基因座在感染Caco - 2细胞中具有不同作用。ail基因座启动细胞黏附，而inv基因座启动细胞黏附及细胞进入过程。此外，我们观察到：（i）当Caco - 2细胞未分化时，细菌细胞黏附（ail）和细菌细胞侵袭（inv）均发生在亚汇合状态，且（ii）当分化开始时，这些过程停止。由于整合素β1异二聚体参与假结核耶尔森菌在几种哺乳动物细胞中的细胞进入过程，我们进一步研究了哪种β1整合素促进假结核耶尔森菌在Caco - 2细胞中的细胞进入。（摘要截短至250字）
