Institute of Microbiology, Department of Biology, ETH Zürich, Zürich, Switzerland.
Science for Life Laboratory, Department of Medical Biochemistry and Microbiology, Uppsala University, Uppsala, Sweden.
PLoS Pathog. 2020 May 4;16(5):e1008503. doi: 10.1371/journal.ppat.1008503. eCollection 2020 May.
Salmonella enterica serovar Typhimurium (S.Tm) infections of cultured cell lines have given rise to the ruffle model for epithelial cell invasion. According to this model, the Type-Three-Secretion-System-1 (TTSS-1) effectors SopB, SopE and SopE2 drive an explosive actin nucleation cascade, resulting in large lamellipodia- and filopodia-containing ruffles and cooperative S.Tm uptake. However, cell line experiments poorly recapitulate many of the cell and tissue features encountered in the host's gut mucosa. Here, we employed bacterial genetics and multiple imaging modalities to compare S.Tm invasion of cultured epithelial cell lines and the gut absorptive epithelium in vivo in mice. In contrast to the prevailing ruffle-model, we find that absorptive epithelial cell entry in the mouse gut occurs through "discreet-invasion". This distinct entry mode requires the conserved TTSS-1 effector SipA, involves modest elongation of local microvilli in the absence of expansive ruffles, and does not favor cooperative invasion. Discreet-invasion preferentially targets apicolateral hot spots at cell-cell junctions and shows strong dependence on local cell neighborhood. This proof-of-principle evidence challenges the current model for how S.Tm can enter gut absorptive epithelial cells in their intact in vivo context.
鼠伤寒沙门氏菌(S.Tm)感染培养的细胞系引发了上皮细胞侵袭的隆起模型。根据该模型,III 型分泌系统-1(TTSS-1)效应蛋白 SopB、SopE 和 SopE2 驱动爆炸性的肌动蛋白成核级联反应,导致大的片状伪足和丝状伪足隆起,并协同 S.Tm 摄取。然而,细胞系实验很难重现宿主肠道黏膜中遇到的许多细胞和组织特征。在这里,我们利用细菌遗传学和多种成像方式比较了 S.Tm 在体内感染培养的上皮细胞系和肠道吸收上皮细胞的情况。与流行的隆起模型相反,我们发现肠道吸收上皮细胞的入侵是通过“离散入侵”发生的。这种独特的入侵方式需要保守的 TTSS-1 效应蛋白 SipA,涉及局部微绒毛的适度伸长,而没有广泛的隆起,并且不有利于协同入侵。离散入侵优先靶向细胞-细胞连接处的顶端侧热点,并且强烈依赖于局部细胞邻域。这一原理验证证据挑战了目前关于 S.Tm 如何在完整的体内环境中进入肠道吸收上皮细胞的模型。