Jensen V B, Harty J T, Jones B D
Department of Microbiology, University of Iowa School of Medicine, Iowa City, Iowa 52242-1109, USA.
Infect Immun. 1998 Aug;66(8):3758-66. doi: 10.1128/IAI.66.8.3758-3766.1998.
Invasive enteric bacteria must pass through the intestinal epithelium in order to establish infection. It is becoming clear that a common target for intestinal mucosa penetration is the specialized epithelial cell of Peyer's patches, the M cell. In order to gain a better understanding of how bacteria interact with M cells, we have compared the interactions of Salmonella typhimurium, Listeria monocytogenes, and Shigella flexneri with M cells by using a murine ligated-loop model. Our results indicate that S. typhimurium possesses a highly efficient mechanism for M cell entry that targets and destroys these cells, while L. monocytogenes and S. flexneri appear to be internalized into M cells in a less disruptive fashion. Early uptake of Listeria or Shigella into M cells appeared to lead to the death of some cells, as evidenced by the appearance of holes in the intestinal epithelium. At later time points, the follicle-associated epithelium of animals infected with these bacteria displayed extensive destruction. These data indicate that enteric pathogens use different strategies to interact with M cells and initiate infection of a host.
侵袭性肠道细菌必须穿过肠上皮细胞才能引发感染。越来越清楚的是,肠道黏膜穿透的一个共同靶点是派尔集合淋巴结的特化上皮细胞,即M细胞。为了更好地了解细菌如何与M细胞相互作用,我们通过使用小鼠结扎肠袢模型,比较了鼠伤寒沙门氏菌、单核细胞增生李斯特菌和福氏志贺氏菌与M细胞的相互作用。我们的结果表明,鼠伤寒沙门氏菌拥有一种高效的进入M细胞的机制,该机制靶向并破坏这些细胞,而单核细胞增生李斯特菌和福氏志贺氏菌似乎以一种破坏性较小的方式被内化到M细胞中。李斯特菌或志贺氏菌早期被M细胞摄取似乎导致了一些细胞的死亡,肠道上皮出现孔洞就是证明。在随后的时间点,感染这些细菌的动物的滤泡相关上皮出现广泛破坏。这些数据表明,肠道病原体使用不同的策略与M细胞相互作用并引发宿主感染。