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Following in Real Time the Impact of Pneumococcal Virulence Factors in an Acute Mouse Pneumonia Model Using Bioluminescent Bacteria
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PavA of Streptococcus pneumoniae modulates adherence, invasion, and meningeal inflammation

Daniela Pracht1, Christine Elm, Joachim Gerber

  • 1Research Center for Infectious Diseases, University of Würzburg, Röntgenring 11, D-97070 Würzburg, Germany.

Infection and Immunity
|April 23, 2005
PubMed

Insights

Pneumococcal adherence and virulence factor A (PavA) is crucial for Streptococcus pneumoniae virulence and colonization. Deleting PavA significantly reduced bacterial adherence, invasion, and meningitis severity in mice.

Area of Science:

  • Microbiology
  • Infectious Diseases
  • Pathogenesis

Background:

  • Pneumococcal adherence and virulence factor A (PavA) is a surface protein of Streptococcus pneumoniae.
  • PavA is essential for pneumococcal virulence in septicemia models.
  • PavA lacks typical signal sequences for cell surface display.

Purpose of the Study:

  • To investigate the role of PavA in pneumococcal adhesion to and invasion of eukaryotic cells.
  • To determine the impact of PavA on experimental pneumococcal meningitis.
  • To elucidate the mechanism by which PavA influences pneumococcal colonization.

Main Methods:

  • Construction and characterization of a pavA knockout mutant of S. pneumoniae D39.
  • Assessment of pneumococcal adherence and internalization by epithelial and endothelial cell lines.
  • Evaluation of bacterial virulence in a mouse model of meningitis.
  • Analysis of the effect of anti-PavA antibodies and PavA protein on pneumococcal attachment.

Main Results:

  • The pavA knockout mutant showed significantly reduced virulence in the mouse meningitis model.
  • PavA-deficient strains exhibited substantially decreased adherence to and internalization by various eukaryotic cell lines.
  • Neither anti-PavA antisera nor exogenous PavA protein restored pneumococcal adherence.
  • Complementation with exogenously added PavA did not restore adherence of the mutant.

Conclusions:

  • PavA plays a critical role in Streptococcus pneumoniae adherence, invasion, and virulence, particularly in meningitis.
  • The mechanism of PavA's action appears to involve modulation of other virulence determinants rather than direct adhesive or invasive functions.
  • PavA is a potential target for therapeutic strategies against pneumococcal infections.

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