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The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a membrane...
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Species-specific interaction of Streptococcus pneumoniae with human complement factor H.

Ling Lu1, Zhuo Ma, T Sakari Jokiranta

  • 1Center for Immunology and Microbial Disease, Albany Medical College, Albany, NY 12208, USA.

Journal of Immunology (Baltimore, Md. : 1950)
|November 5, 2008
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Streptococcus pneumoniae evades human immune defenses by using its CbpA protein to bind human complement factor H (FH). This interaction, specific to humans, helps the bacteria resist complement-mediated clearance, preventing bacterial clearance.

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Area of Science:

  • Microbiology
  • Immunology
  • Molecular Biology

Background:

  • Streptococcus pneumoniae colonizes the nasopharynx and can cause invasive infections.
  • Pneumococcal immune evasion involves resisting host innate immunity.
  • Complement factor H (FH) inhibits the complement alternative pathway, aiding bacterial survival.

Purpose of the Study:

  • To investigate the species-specific interaction between Streptococcus pneumoniae's CbpA and complement factor H.
  • To determine the role of CbpA in pneumococcal resistance to host immune defenses.

Main Methods:

  • Investigated CbpA binding to human and animal FH proteins.
  • Utilized a mouse model to assess virulence of CbpA-mutated S. pneumoniae.
  • Performed phagocytosis assays with human and mouse phagocytes and complement systems.

Main Results:

  • CbpA specifically binds human FH, but not FH from other tested species.
  • Deletion of the FH binding domain in CbpA did not alter pneumococcal bacteremia or virulence in mice.
  • Species-specific FH interaction was observed in clinical pneumococcal isolates.
  • Phagocytosis experiments confirmed CbpA's role in resisting human complement-mediated defense.

Conclusions:

  • CbpA mediates species-specific binding of FH by Streptococcus pneumoniae.
  • This interaction is a key mechanism for pneumococcal immune evasion in humans.
  • CbpA is a determinant of pneumococcal resistance to human complement-mediated host defense.