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Streptococcus pyogenes serotype M1 encodes multiple pathways for entry into human epithelial cells

D Cue1, P E Dombek, H Lam

  • 1Department of Microbiology, University of Minnesota, Minneapolis, Minnesota, USA.

Infection and Immunity
|September 24, 1998
PubMed
Summary
This summary is machine-generated.

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Streptococcus pyogenes M1 protein mediates invasion of lung cells through interactions with host cell fibronectin and laminin. Multiple invasion pathways exist, involving M1 protein, host integrins, and their ligands.

Area of Science:

  • Microbiology
  • Cell Biology
  • Infectious Diseases

Background:

  • Streptococcus pyogenes serotype M1 invasion of lung epithelial cells is serum protein-dependent.
  • The M1 protein's role in this invasion process requires further elucidation.

Purpose of the Study:

  • To investigate the role of the M1 protein in Streptococcus pyogenes invasion of A549 human lung epithelial cells.
  • To determine the specific host cell factors and bacterial mechanisms involved in M1-mediated invasion.

Main Methods:

  • Comparison of invasion and adherence of M1-positive and M1-negative S. pyogenes strains with various agonists (FBS, Fn, Lm, RGD peptides).
  • Analysis of fibronectin binding to M1 protein and M1-deficient mutants.
  • Inhibition studies using anti-integrin monoclonal antibodies (MAbs) against host cell receptors.

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Main Results:

  • M1 protein expression significantly enhanced invasion (up to 70-fold) and adherence stimulated by FBS, Fn, and Lm.
  • M1-negative strains showed reduced invasion and adherence, with Fn binding decreased by 88%.
  • Anti-integrin beta1 and alpha5beta1 antibodies inhibited specific invasion pathways, suggesting involvement of host integrins.

Conclusions:

  • Streptococcus pyogenes M1 protein is crucial for invasion mediated by fibronectin and laminin.
  • Multiple invasion mechanisms exist, involving M1 protein, host integrins (like beta1 and alpha5beta1), and their ligands.
  • These findings highlight complex bacterial-host interactions in S. pyogenes pathogenesis.