Encapsulated group B S treptococcus modulates dendritic cell functions via lipid rafts and clathrin‐mediated endocytosis

Summary Group B S treptococcus ( 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 ( DC s) 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 DC s. 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 DC s 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 CCL 2 by DC s 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 DC s, which was selectively modulated by the presence of CPS .