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Neisseria meningitidis pili induce type-IIA phospholipase A2 expression in alveolar macrophages

Lhousseine Touqui1, Miguel Paya, Françoise Thouron

  • 1Unité de Défense Innée et Inflammation, Inserm E-336, Institut Pasteur, 25 rue du Dr. Roux, 75015 Paris, France. touqui@pasteur.fr

FEBS Letters
|August 24, 2005
PubMed

Insights

Bacterial pili, not just lipooligosaccharide, trigger alveolar macrophages to produce type-IIA secreted phospholipase A2 (sPLA2-IIA) via a nuclear factor kappa B (NF-kappaB) pathway.

Area of Science:

  • Immunology
  • Microbiology
  • Molecular Biology

Background:

  • Type-IIA secreted phospholipase A2 (sPLA2-IIA) plays a role in inflammatory responses.
  • The induction of sPLA2-IIA by bacterial components beyond lipopolysaccharide (LPS) is not well understood.

Purpose of the Study:

  • To investigate the role of Neisseria meningitidis components, particularly pili, in inducing sPLA2-IIA expression in alveolar macrophages (AM).

Main Methods:

  • Exposure of AM to wild-type and mutant strains of N. meningitidis, including lipooligosaccharide (LOS)-deficient and pili-defective mutants.
  • Analysis of sPLA2-IIA synthesis and nuclear factor kappa B (NF-kappaB) activation.

Main Results:

  • Both wild-type N. meningitidis and its LOS induced sPLA2-IIA synthesis in AM.
  • A mutant lacking LOS still induced sPLA2-IIA, indicating other factors are involved.
  • Pili isolated from a LOS-defective strain induced sPLA2-IIA expression and NF-kappaB activation, suggesting pili are key inducers.

Conclusions:

  • Bacterial pili are potent inducers of sPLA2-IIA expression in alveolar macrophages.
  • This induction occurs through a NF-kappaB-dependent signaling pathway.

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