Reed K A, Clark M A, Booth T A, Hueck C J, Miller S I, Hirst B H, Jepson M A
Department of Physiological Sciences, Medical School, University of Newcastle upon Tyne, United Kingdom.
Infect Immun. 1998 May;66(5):2007-17. doi: 10.1128/IAI.66.5.2007-2017.1998.
The formation of filamentous appendages on Salmonella typhimurium has been implicated in the triggering of bacterial entry into host cells (C. C. Ginocchio, S. B. Olmsted, C. L. Wells, and J. E. Galán, Cell 76:717-724, 1994). We have examined the roles of cell contact and Salmonella pathogenicity island 1 (SPI1) in appendage formation by comparing the surface morphologies of a panel of S. typhimurium strains adherent to tissue culture inserts, to cultured epithelial cell lines, and to murine intestine. Scanning electron microscopy revealed short filamentous appendages 30 to 50 nm in diameter and up to 300 nm in length on many wild-type S. typhimurium bacteria adhering to both cultured epithelial cells and to murine Peyer's patch follicle-associated epithelia. Wild-type S. typhimurium adhering to cell-free culture inserts lacked these filamentous appendages but sometimes exhibited very short appendages which might represent a rudimentary form of the cell contact-stimulated filamentous appendages. Invasion-deficient S. typhimurium strains carrying mutations in components of SPI1 (invA, invG, sspC, and prgH) exhibited filamentous appendages similar to those on wild-type S. typhimurium when adhering to epithelial cells, demonstrating that formation of these appendages is not itself sufficient to trigger bacterial invasion. When adhering to cell-free culture inserts, an S. typhimurium invG mutant differed from its parent strain in that it lacked even the shorter surface appendages, suggesting that SPI1 may be involved in appendage formation in the absence of epithelia. Our data on S. typhimurium strains in the presence of cells provide compelling evidence that SPI1 is not an absolute requirement for the formation of the described filamentous appendages. However, appendage formation is controlled by PhoP/PhoQ since a PhoP-constitutive mutant very rarely possessed such appendages when adhering to any of the cell types examined.
鼠伤寒沙门氏菌丝状附属物的形成与细菌进入宿主细胞的触发过程有关（C.C.吉诺基奥、S.B.奥尔姆斯特德、C.L.韦尔斯和J.E.加兰，《细胞》76:717 - 724，1994年）。我们通过比较一组粘附于组织培养插入物、培养的上皮细胞系和小鼠肠道的鼠伤寒沙门氏菌菌株的表面形态，研究了细胞接触和沙门氏菌致病岛1（SPI1）在附属物形成中的作用。扫描电子显微镜显示，许多粘附于培养的上皮细胞和小鼠派伊尔结滤泡相关上皮的野生型鼠伤寒沙门氏菌细菌上有直径为30至50纳米、长度达300纳米的短丝状附属物。粘附于无细胞培养插入物的野生型鼠伤寒沙门氏菌没有这些丝状附属物，但有时会表现出非常短的附属物，这可能代表细胞接触刺激的丝状附属物的一种原始形式。携带SPI1组分（invA、invG、sspC和prgH）突变的侵袭缺陷型鼠伤寒沙门氏菌菌株在粘附于上皮细胞时表现出与野生型鼠伤寒沙门氏菌相似的丝状附属物，这表明这些附属物的形成本身不足以触发细菌侵袭。当粘附于无细胞培养插入物时，鼠伤寒沙门氏菌invG突变体与其亲本菌株的不同之处在于它甚至没有较短的表面附属物，这表明SPI1可能在没有上皮细胞的情况下参与附属物的形成。我们关于存在细胞时鼠伤寒沙门氏菌菌株的数据提供了令人信服的证据，即SPI1不是所述丝状附属物形成的绝对必要条件。然而，附属物的形成受PhoP/PhoQ控制，因为组成型PhoP突变体在粘附于任何所检测的细胞类型时很少拥有这种附属物。
