Clark M A, Reed K A, Lodge J, Stephen J, Hirst B H, Jepson M A
Department of Physiological Sciences, Medical School, University of Newcastle upon Tyne, United Kingdom.
Infect Immun. 1996 Oct;64(10):4363-8. doi: 10.1128/iai.64.10.4363-4368.1996.
We have examined the role of the Salmonella typhimurium inv locus in invasion of the murine intestine. Previous studies have demonstrated that M cells within the lymphoid-follicle-associated epithelia are the primary site of intestinal invasion by S. typhimurium. In this study, we show that mutants possessing defects in one of two inv genes, invA or invG, which render them severely deficient for invasion of polarized epithelial MDCK cells, retain their ability to actively invade mouse Peyer's patch M cells. The interaction of these mutants with M cells was associated with apical membrane remodelling resembling that induced by wild-type strains. These data demonstrate that Salmonella invasion in vivo can proceed via mechanisms other than those previously defined in cultured cells.
我们研究了鼠伤寒沙门氏菌inv基因座在侵袭小鼠肠道中的作用。先前的研究表明，淋巴滤泡相关上皮内的M细胞是鼠伤寒沙门氏菌肠道侵袭的主要部位。在本研究中，我们发现，在两个inv基因（invA或invG）之一中存在缺陷的突变体，使其对极化上皮MDCK细胞的侵袭严重不足，但仍保留主动侵袭小鼠派尔集合淋巴结M细胞的能力。这些突变体与M细胞的相互作用与顶端膜重塑有关，类似于野生型菌株诱导的情况。这些数据表明，沙门氏菌在体内的侵袭可以通过不同于先前在培养细胞中定义的机制进行。
