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Invasion of Human Cells by a Bacterial Pathogen
07:15

Invasion of Human Cells by a Bacterial Pathogen

Published on: March 21, 2011

M protein mediated adhesion of M type 24 Streptococcus pyogenes stimulates release of interleukin-6 by HEp-2 tissue

H S Courtney1, I Ofek, D L Hasty

  • 1Veterans Affairs Medical Center, University of Tennessee, Memphis, USA. hcourtney@utmem1.utmem.edu

FEMS Microbiology Letters
|June 1, 1997
PubMed

Insights

Lipoteichoic acid mediates reversible adhesion of group A streptococci, while M protein is crucial for irreversible attachment and interleukin-6 release. This clarifies bacterial adhesion mechanisms.

Area of Science:

  • Microbiology
  • Immunology
  • Cell Biology

Background:

  • Group A Streptococcus (GAS) adhesion is critical for infection.
  • Understanding the roles of specific GAS surface components is essential for developing targeted therapies.

Purpose of the Study:

  • To elucidate the distinct contributions of lipoteichoic acid and M protein to GAS adhesion.
  • To investigate the impact of GAS adhesion on host cell interleukin-6 (IL-6) release.

Main Methods:

  • Investigated adhesion of encapsulated and unencapsulated GAS strains with varying M protein and lipoteichoic acid expression to HEp-2 cells.
  • Quantified bacterial attachment and detachment through multiple washing steps.
  • Assessed IL-6 release from HEp-2 cells in response to GAS interaction.

Main Results:

  • Hyaluronate-masked GAS showed no attachment, indicating capsule's role in preventing initial contact.
  • M-negative GAS with exposed lipoteichoic acid exhibited loose, reversible attachment.
  • GAS expressing both lipoteichoic acid and M protein demonstrated stable, irreversible adhesion.
  • GAS expressing both M protein and lipoteichoic acid induced significant IL-6 release, unlike M-negative mutants.

Conclusions:

  • Lipoteichoic acid mediates the initial, reversible adhesion of GAS to host cells.
  • M protein is essential for irreversible adhesion and subsequent induction of IL-6 release.
  • These findings highlight the specific roles of GAS surface proteins in pathogenesis and host immune response.

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