Zychlinsky A, Perdomo J J, Sansonetti P J
Unité de Pathogénie Microbienne Moléculaire, INSERM U199, Paris, France.
Ann N Y Acad Sci. 1994 Aug 15;730:197-208. doi: 10.1111/j.1749-6632.1994.tb44249.x.
Shigella flexneri, a member of the family of enterobacteriaceae, causes bacillary dysentery by invading the human colonic mucosa and provoking a very intense inflammation. Recent in vitro data allow us to integrate different phenomena into a model of the infectious process during shigellosis. In vivo, bacteria appear to enter the submucosa via the M cells, specialized cells that cover the follicular structures of the intestinal mucosa. Once inside the submucosa, shigellae encounter resident tissue macrophages, which are infected, and apoptosis is rapidly induced. During programmed cell death the inflammatory cytokine interleukin-1 (IL-1) is released. Interleukin-1 triggers an inflammatory reaction characterized by extravasation of polymorphonuclear (PMN) cells. The inflammation is probably potentiated by the production of other cytokines by epithelial, endothelial, and PMN cells. Polymorphonuclear cells migrate through the epithelium into the lumen of the colon, destabilizing the integrity of the epithelial barrier. The damaged epithelium allows massive entry of bacteria into the submucosa. Further colonization of the epithelium aggravates inflammation, which in turn causes extensive tissue destruction. Both the in vitro and in vivo results that support this model are discussed.
福氏志贺菌是肠杆菌科的一员，通过侵入人类结肠黏膜并引发强烈炎症而导致细菌性痢疾。最近的体外实验数据使我们能够将不同现象整合到志贺菌病感染过程的模型中。在体内，细菌似乎通过M细胞进入黏膜下层，M细胞是覆盖肠黏膜滤泡结构的特殊细胞。一旦进入黏膜下层，志贺菌会遇到驻留组织巨噬细胞并将其感染，随后迅速诱导细胞凋亡。在程序性细胞死亡过程中，炎性细胞因子白细胞介素-1（IL-1）被释放。白细胞介素-1引发以多形核（PMN）细胞渗出为特征的炎症反应。上皮细胞、内皮细胞和PMN细胞产生的其他细胞因子可能会增强炎症反应。多形核细胞通过上皮迁移到结肠腔，破坏上皮屏障的完整性。受损的上皮使得细菌大量进入黏膜下层。上皮的进一步定植加剧炎症，进而导致广泛的组织破坏。本文将讨论支持该模型的体外和体内实验结果。
