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Invasion of Human Cells by a Bacterial Pathogen
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Invasion of Human Cells by a Bacterial Pathogen

Published on: March 21, 2011

Immunoglobulins inhibit adherence and internalization of Streptococcus pyogenes to human pharyngeal cells

U Fluckiger1, V A Fischetti

  • 1Rockefeller University, New York, New York 10021, USA.

Advances in Experimental Medicine and Biology
|January 1, 1997
PubMed

Insights

Human secretory IgA antibodies effectively block Group A Streptococcus adherence to throat cells. However, the M protein is crucial for bacterial invasion, not initial adherence, and can be targeted by specific antibodies.

Area of Science:

  • Microbiology
  • Immunology
  • Infectious Diseases

Background:

  • Group A Streptococcus (GAS) is a significant human pathogen.
  • The M protein is a key virulence factor in GAS, but its role in adherence and invasion is debated.
  • Secretory IgA (sIgA) is the primary antibody in mucosal secretions and plays a role in mucosal immunity.

Purpose of the Study:

  • To investigate the role of human sIgA in Group A Streptococcus adherence to pharyngeal cells.
  • To determine the involvement of the M protein in GAS adherence and invasion of human pharyngeal cells.
  • To assess the efficacy of antibodies targeting the M protein in blocking GAS internalization.

Main Methods:

  • Purified human sIgA was used to test inhibition of GAS adherence to pharyngeal cells.
  • Rabbit antisera against whole M+ strain and recombinant M6 protein were employed.
  • Isogenic M- derivative strains were used to compare invasion capabilities.
  • Inhibition of bacterial internalization by specific antisera was analyzed.

Main Results:

  • Human sIgA significantly inhibited GAS adherence to pharyngeal cells.
  • Rabbit antiserum against the whole M+ strain did not inhibit adherence.
  • The M protein likely does not mediate GAS adherence to respiratory cells.
  • An isogenic M- derivative showed reduced invasion, suggesting M protein's role in internalization.
  • Rabbit serum against recombinant M6 protein blocked GAS internalization, but not adherence.

Conclusions:

  • Human sIgA plays a protective role against GAS adherence.
  • The M protein is primarily involved in the internalization of GAS into host cells, rather than initial adherence.
  • Targeting the M protein via specific antibodies may be a viable strategy to prevent GAS infection by blocking invasion.

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