Contribution of Streptococcus pyogenes M87 protein to innate immune resistance and virulence. (August 2022)

• Record Type: Journal Article
• Authors: Hirose, Yujiro; Kolesinski, Piotr; Hiraoka, Masanobu; Uchiyama, Satoshi; Zurich, Raymond H.; Kumaraswamy, Monika; Bjanes, Elisabet; Ghosh, Partho; Kawabata, Shigetada; Nizet, Victor
• Is Part Of: Microbial pathogenesis. Volume 169(2022)
• Publication Date: 2022-08
• Subjects: Streptococcus pyogenes -- emm87 -- M protein -- Virulence factor; Pathogenic microorganisms -- Periodicals; Pathology, Molecular -- Periodicals; Communicable Diseases -- microbiology -- Periodicals; Communicable Diseases -- parasitology -- Periodicals; Micro-organismes pathogènes -- Périodiques; Pathologie moléculaire -- Périodiques; Electronic journals; 616.9041
• DOI: 10.1016/j.micpath.2022.105636
• Languages: English
• ISSNs: 0882-4010

Abstract

Abstract: Streptococcus pyogenes is a pre-eminent human pathogen, and classified by the hypervariable sequence of the emm gene encoding the cell surface M protein . Among a diversity of M/ emm types, the prevalence of the M/ emm 87 strain has been steadily increasing in invasive S. pyogenes infections. Although M protein is the major virulence factor for globally disseminated M/ emm 1 strain, it is unclear if or how the corresponding M protein of M/ emm 87 strain (M87 protein) functions as a virulence factor. Here, we use targeted mutagenesis to show that the M87 protein contributes to bacterial resistance to neutrophil and whole blood killing and promotes the release of mature IL-1β from macrophages. While deletion of emm87 did not influence epithelial cell adherence and nasal colonization, it significantly reduced S. pyogenes -induced mortality and bacterial loads in a murine systemic infection model. Our data suggest that emm87 is involved in pathogenesis by modulating the interaction between S. pyogenes and innate immune cells. Highlights: M/ emm 87 strains are increasing in invasive Streptococcus pyogenes epidemiology. M87 protein contributes to bacterial resistance to neutrophil and whole blood killing. M87 protein promotes the release of mature IL-1β from macrophages. Deletion of emm87 did not influence epithelial cell adherence and nasal colonization. Deletion of emm87 reduced mortality and bacterial loads in murine systemic infection.