AI Article Synopsis

  • Tissue injury and ECM degradation are significant features of group A Streptococcus (GAS) skin infections, largely influenced by M proteins with lectin-like abilities.
  • The study found that M proteins from different GAS strains bind to hyaluronic acid through specific motifs, which affects keratinocyte wound healing negatively.
  • Understanding the interaction between hyaluronic acid and M proteins could help develop new nonantibiotic treatments to combat GAS skin infections by improving ECM composition and healing responses.

Article Abstract

Tissue injury, including extracellular matrix (ECM) degradation, is a hallmark of group A Streptococcus (GAS) skin infection and is partially mediated by M proteins which possess lectin-like properties. Hyaluronic acid is a glycosaminoglycan enriched in the cutaneous ECM, yet an interaction with M proteins has yet to be explored. This study revealed that hyaluronic acid binding was conserved across phylogenetically diverse M proteins, mediated by RR/SR motifs predominantly localized in the C repeat region. Keratinocyte wound healing was decreased through the recruitment of hyaluronic acid by M proteins in an M type-specific manner. GAS strains 5448 (M1 serotype) and ALAB49 (M53 serotype) also bound hyaluronic acid via M proteins, but hyaluronic acid could increase bacterial adherence independently of M proteins. The identification of host-pathogen mechanisms that affect ECM composition and cell repair responses may facilitate the development of nonantibiotic therapeutics that arrest GAS disease progression in the skin.

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Source
http://dx.doi.org/10.1096/fj.202401301RDOI Listing

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