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Interactions between Bordetella pertussis and the complement inhibitor factor H.

Hanne Amdahl1, Hanna Jarva, Marjo Haanperä

  • 1Department of Bacteriology and Immunology, Haartman Institute, University of Helsinki, Helsinki, Finland.

Molecular Immunology
|December 21, 2010
PubMed
Summary

Bordetella pertussis and B. parapertussis evade the alternative complement pathway by binding host factor H (FH). This binding prevents complement attack, aiding bacterial survival and contributing to whooping cough persistence.

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Area of Science:

  • Immunology
  • Microbiology
  • Bacteriology

Background:

  • Whooping cough (pertussis) is a highly contagious respiratory illness caused by Bordetella pertussis.
  • Despite childhood immunization, rising cases in adolescents and adults highlight the need to understand bacterial evasion mechanisms.
  • The complement system is a crucial innate immunity defense against bacterial pathogens.

Purpose of the Study:

  • To investigate how Bordetella pertussis and B. parapertussis evade the alternative complement pathway.
  • To identify bacterial surface mechanisms for resisting complement-mediated killing.
  • To determine if clinical isolates differ in complement evasion strategies compared to reference strains.

Main Methods:

  • Survival assays in fresh non-immune human serum.
  • Adsorption assays and flow cytometry to detect bacterial surface binding.
  • Radioligand binding assays to quantify factor H (FH) interaction.
  • Identification of FH binding regions using deletion mutants.

Main Results:

  • Clinical isolates of B. pertussis and B. parapertussis survived alternative complement pathway attack better than the reference strain.
  • Both species efficiently bound the complement regulator factor H (FH) from normal human serum.
  • Bound FH retained its regulatory function, promoting C3b cleavage and inhibiting complement activation.
  • FH binding primarily involved its C-terminal short consensus repeat domains 19-20.
  • The avian pathogen B. avium did not bind FH and was susceptible to complement.

Conclusions:

  • B. pertussis and B. parapertussis employ surface acquisition of human factor H (FH) to evade the alternative complement pathway.
  • This mechanism allows the bacteria to resist complement-mediated killing, facilitating host colonization.
  • FH acquisition represents a key virulence strategy for these Bordetella species.