Group B Streptococcus (GBS) is an important agent of life-threatening invasive infection.It has been previously shown that encapsulated type III GBS is easily internalized by dendritic cells (DCs), and that this internalization had an impact on cytokine Ball - Glove Baseball Catcher - Senior production.The receptors underlying these processes are poorly characterized.
Knowledge on the mechanisms used by type V GBS to activate DCs is minimal.In this work, we investigated the role of Toll-like receptor (TLR)/MyD88 signaling pathway, the particular involvement of TLR2, and that of the intracellular sensing receptor NOD2 in the activation of DCs by types III and V GBS.The role of capsular polysaccharide (CPS, one of the most important GBS virulence factors) in bacterial-DC interactions was evaluated using non-encapsulated mutants.
Despite differences in the role of CPS between types III and V GBS in bacterial internalization and Vehicle Lights intracellular survival, no major differences were observed in their capacity to modulate release of cytokines by DC.For both serotypes, CPS had a minor role in this response.Production of cytokines by DCs was shown to strongly rely on MyD88-dependent signaling pathways, suggesting that DCs recognize GBS and become activated mostly through TLR signaling.
Yet, GBS-infected TLR2-/- DCs only showed a partial reduction in the production of IL-6 and CXCL1 compared to control DCs.Surprisingly, CXCL10 release by type III or type V GBS-infected DCs was MyD88-independent.No differences in DC activation were observed between NOD2-/- and control DCs.
These results demonstrate the involvement of various receptors and the complexity of the cytokine production pathways activated by GBS upon DC infection.