A teichoic acid-like wall modification associated with immune suppression is socially regulated in Streptococcus pyogenes

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Streptococcus pyogenes (group A streptococcus [GAS]) is a human-restricted pathogen with a range of clinical manifestations and worldwide prevalence. The GAS Rgg2/Rgg3 quorum-sensing (QS) system, a cell-to-cell communication network, modifies the cell surface, resulting in increased lysozyme resistance, biofilm formation, and expression of the qim operon which is responsible for modulation of innate immune responses in macrophages. The operon encodes 10 genes with predicted homology to enzymes involved in bacterial cell surface-associated carbohydrate and teichoic acid biosynthesis pathways. Comparing extracts of GAS cell wall polysaccharides between wild type and operon mutants showed that QS-induced genes modify the S. pyogenes cell surface by adding a wall teichoic acid-like N-acetylglucosamine-linked ribitol (GlcNAc-Rbo) moiety. A fluorescently labeled phage receptor-binding protein, RBP-13-GFP, that recognizes GlcNAc-decorated ribitol phosphate repeats, bound to the GAS surface only when qim expression was induced. Deletion of the qim operon eliminated RBP-13-GFP binding, diminished bacterial colonization, and significantly attenuated GAS pathogenesis in a murine skin infection model. These findings indicate that GAS has evolved a strategy to evade innate immune response by presenting a previously unknown carbohydrate moiety upon QS.

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