Laboratory of Immunology, Université de Montréal, St-Hyacinthe, Quebec, Canada.
Cell Microbiol. 2012 Nov;14(11):1707-19. doi: 10.1111/j.1462-5822.2012.01830.x. Epub 2012 Jul 11.
Group B Streptococcus (GBS) capsular type III is an important agent of life-threatening invasive infections. It has been previously shown that encapsulated GBS is easily internalized by dendritic cells (DCs) and can persist inside these immune cells. The mechanisms underlying these processes are unknown. Here, colocalization studies and the use of endocytosis inhibitors and caveolin(-/-) mice, demonstrated that GBS uses multiple endocytosis mechanisms to enter mouse DCs. The capsular polysaccharide (CPS) selectively drives GBS internalization via caveolae-independent but lipid raft-dependent pathways. Non-encapsulated bacteria failed to engage lipid rafts. GBS internalization by DCs also occurs via clathrin-mediated endocytosis in a process independent of bacterial CPS. Albeit caveolae are not required for GBS internalization, signalling events through caveolin-1 are involved in production of the inflammatory chemokine CCL2 by DCs infected with encapsulated GBS only. This study addresses for the first time endocytosis pathways implicated in DC internalization of encapsulated GBS and suggests a complex interplay between GBS and DCs, which was selectively modulated by the presence of CPS.
B 群链球菌（GBS）荚膜型 III 是一种导致严重威胁生命的侵袭性感染的重要病原体。此前已经表明，带荚膜的 GBS 很容易被树突状细胞（DC）内化，并能在这些免疫细胞内持续存在。这些过程背后的机制尚不清楚。在这里，通过共定位研究以及使用内吞作用抑制剂和小窝蛋白（-/-）小鼠，证明 GBS 使用多种内吞作用机制进入小鼠 DC。荚膜多糖（CPS）通过非网格蛋白但依赖于脂筏的途径选择性地驱动 GBS 的内化。未包裹的细菌无法与脂筏结合。通过 DC 的 CPS 独立的网格蛋白介导的内吞作用也会发生 GBS 内化。虽然小窝不需要 GBS 的内化，但仅在感染有荚膜的 GBS 的 DC 中，通过小窝蛋白-1 的信号事件参与炎性趋化因子 CCL2 的产生。本研究首次解决了与 DC 内化包裹 GBS 相关的内吞作用途径，并表明 GBS 和 DC 之间存在复杂的相互作用，这种相互作用被 CPS 的存在选择性地调节。
