Sansonetti P J, Tran Van Nhieu G, Egile C
Unité de Pathogénie Microbienne Moléculaire, Institut National de la Santé et de la Recherche Médicale, Institut Pasteur, Paris, France.
Clin Infect Dis. 1999 Mar;28(3):466-75. doi: 10.1086/515150.
Invasion of the intestinal barrier by Shigella flexneri involves complex interactions with epithelial and phagocytic cells. Major perturbation of the signals that maintain epithelial integrity permits mucosal invasion, leading to tissue destruction. Expression of this invasive phenotype depends on the secretion of Ipa proteins (invasins), which can trigger entry of the pathogen into epithelial cells by causing massive rearrangement of the host cell cytoskeleton and cause macrophage apoptotic death by direct interaction of IpaB with interleukin-1beta (IL-1beta)-converting enzyme. This results in the killing of defense cells and in the release of IL-1beta. In vivo, bacteria translocate through the epithelial barrier, essentially via M cells of the follicle-associated epithelium in the colonic and rectal mucosa. Apoptotic death of macrophages in subepithelial tissues allows bacterial survival and triggers inflammation, which destabilizes epithelial structures and facilitates further bacterial entry. Once they are intracellular, bacteria multiply within the cytoplasm and move from cell to cell by an actin-dependent process.
福氏志贺菌对肠道屏障的侵袭涉及与上皮细胞和吞噬细胞的复杂相互作用。维持上皮完整性的信号发生重大扰动会导致黏膜侵袭，进而造成组织破坏。这种侵袭性表型的表达取决于Ipa蛋白（侵袭素）的分泌，Ipa蛋白可通过引起宿主细胞细胞骨架的大量重排来触发病原体进入上皮细胞，并通过IpaB与白细胞介素-1β（IL-1β）转化酶的直接相互作用导致巨噬细胞凋亡死亡。这会导致防御细胞死亡并释放IL-1β。在体内，细菌主要通过结肠和直肠黏膜中滤泡相关上皮的M细胞穿过上皮屏障。上皮下组织中巨噬细胞的凋亡死亡使细菌得以存活并引发炎症，炎症会破坏上皮结构并促进细菌进一步侵入。一旦进入细胞内，细菌就在细胞质中繁殖，并通过肌动蛋白依赖性过程在细胞间移动。
