Bierne Hélène, Cossart Pascale
Unité des Interactions Bactéries-Cellules, Institut Pasteur, 28 Rue du Docteur Roux, 75724 Paris cedex 15, France.
J Cell Sci. 2002 Sep 1;115(Pt 17):3357-67. doi: 10.1242/jcs.115.17.3357.
Molecules from some pathogenic bacteria mimic natural host cell ligands and trigger engulfment of the bacterium after specifically interacting with cell-surface receptors. The leucine-rich repeat (LRR)-containing protein InlB of Listeria monocytogenes is one such molecule. It triggers bacterial entry by interacting with the hepatocyte growth factor receptor (HGF-R or Met) and two other cellular components: gC1q-R and proteoglycans. Recent studies point to significant similarities between the molecular mechanisms underlying InlB-mediated entry into cells and classic phagocytosis. In addition, InlB, in common with HGF, activates signaling cascades that are not involved in bacterial entry. Therefore, studies of InlB may help us to analyze the previously noticed similarities between growth factor receptor activation and phagocytosis.
一些致病细菌的分子会模拟天然宿主细胞配体,并在与细胞表面受体特异性相互作用后触发细菌的吞噬作用。单核细胞增生李斯特菌中富含亮氨酸重复序列(LRR)的蛋白InlB就是这样一种分子。它通过与肝细胞生长因子受体(HGF-R或Met)以及其他两种细胞成分:gC1q-R和蛋白聚糖相互作用来触发细菌进入细胞。最近的研究表明,InlB介导的细胞进入机制与经典吞噬作用的分子机制之间存在显著相似性。此外,与HGF一样,InlB会激活不参与细菌进入的信号级联反应。因此,对InlB的研究可能有助于我们分析之前注意到的生长因子受体激活与吞噬作用之间的相似性。