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Published on: August 19, 2016

M1 protein allows Group A streptococcal survival in phagocyte extracellular traps through cathelicidin inhibition

Xavier Lauth1, Maren von Köckritz-Blickwede, Case W McNamara

  • 1Department of Pediatrics, University of California San Diego, La Jolla, Calif. 92093-0687, USA.

Journal of Innate Immunity
|April 9, 2010
PubMed

Insights

Group A Streptococcus M1 protein aids pathogen survival by resisting neutrophil extracellular traps and the antimicrobial peptide LL-37. This resistance contributes to M1 strains causing severe invasive infections.

Area of Science:

  • Microbiology
  • Immunology
  • Infectious Diseases

Background:

  • Group A Streptococcus (GAS) M1 protein is known for systemic virulence, interfering with phagocytosis and causing inflammation.
  • Neutrophil and mast cell extracellular traps are innate immune structures that trap and kill pathogens.

Purpose of the Study:

  • To investigate the role of M1 protein in the formation and survival within neutrophil and mast cell extracellular traps.
  • To determine if M1 protein confers resistance to antimicrobial peptides within these traps.
  • To correlate M1 protein's cathelicidin resistance with GAS invasive disease severity.

Main Methods:

  • Targeted mutagenesis and heterologous expression of M1 protein.
  • Assays to assess M1 protein's effect on extracellular trap formation and pathogen survival.
  • Studies on M1 protein fragment inhibition of the antimicrobial peptide LL-37.
  • Survey of clinical GAS isolates for cathelicidin resistance.

Main Results:

  • M1 protein stimulates neutrophil and mast cell extracellular trap formation but promotes GAS survival within them.
  • M1 protein confers resistance to the human cathelicidin antimicrobial peptide LL-37.
  • The N-terminal domain of M1 protein is responsible for inhibiting LL-37.
  • GAS strains from invasive infections (necrotizing fasciitis, toxic shock syndrome) showed higher cathelicidin resistance, with M1 isolates being uniformly resistant.

Conclusions:

  • M1 protein enhances GAS survival in extracellular traps by resisting LL-37.
  • Increased resistance to cathelicidin and extracellular traps contributes to the invasive potential of M1 GAS strains.
  • M1 protein is a key factor in the pathogenesis of severe GAS infections.

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