Ménard R, Prévost M C, Gounon P, Sansonetti P, Dehio C
Unité de Pathogénic Microbienne Moléculaire, Paris, France.
Proc Natl Acad Sci U S A. 1996 Feb 6;93(3):1254-8. doi: 10.1073/pnas.93.3.1254.
The bacterial pathogen Shigella flexneri causes bacillary dysentery in humans by invading coloncytes. Upon contact with epithelial cells, S. flexneri elicits localized plasma membrane projections sustained by long actin filaments which engulf the microorganism. The products necessary for Shigella entry include three secretory proteins: IpaB, IpaC, and IpaD. Extracellular IpaB and IpaC associate in a soluble complex, the Ipa complex. We have immunopurified this Ipa complex on latex beads and found that they were efficiently internalized into HeLa cells. Like S. flexneri entry, uptake of the beads bearing the Ipa complex was associated with membrane projections and polymerization of actin at the site of cell-bead interaction and was dependent on small Rho GTPases. These results indicate that a secreted factor can promote S. flexneri entry into epithelial cells.
细菌病原体福氏志贺菌通过侵入结肠细胞导致人类患细菌性痢疾。与上皮细胞接触后,福氏志贺菌引发由长肌动蛋白丝支撑的局部质膜突起,这些突起会吞噬微生物。志贺菌进入细胞所需的产物包括三种分泌蛋白:IpaB、IpaC和IpaD。细胞外的IpaB和IpaC形成一种可溶性复合物,即Ipa复合物。我们在乳胶珠上免疫纯化了这种Ipa复合物,发现它们能有效地内化到HeLa细胞中。与福氏志贺菌进入细胞一样,携带Ipa复合物的珠子的摄取与膜突起以及细胞与珠子相互作用部位的肌动蛋白聚合有关,并且依赖于小Rho GTP酶。这些结果表明,一种分泌因子可以促进福氏志贺菌进入上皮细胞。