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Complexity and complementarity of outer membrane protein A recognition by cellular and humoral innate immunity

Pascale Jeannin1, Barbara Bottazzi, Marina Sironi

  • 1Centre d'Immunologie Pierre Fabre, 5 Avenue Napoléon III, 74164 Saint-Julien en Genevois, France.

Immunity
|May 17, 2005
PubMed

Insights

Outer membrane protein A from Klebsiella pneumoniae activates immune cells via scavenger receptors and TLR2. This triggers PTX3 production, amplifying the innate immune response against pathogens.

Area of Science:

  • Immunology
  • Microbiology
  • Molecular Biology

Background:

  • Outer membrane protein A (OmpA) is a key component of Enterobacteriaceae outer membranes.
  • Klebsiella pneumoniae OmpA (KpOmpA) interaction with innate immune cells is not fully understood.

Purpose of the Study:

  • To elucidate the mechanism of KpOmpA recognition by innate immune cells.
  • To investigate the role of Toll-like receptor 2 (TLR2) and scavenger receptors (SRs) in KpOmpA-mediated immune activation.

Main Methods:

  • Cellular assays using macrophages and dendritic cells (DCs).
  • Analysis of receptor binding, including scavenger receptors LOX-1 and SREC-I.
  • Investigation of TLR2 signaling pathways and PTX3 production.
  • In vivo studies using TLR2(-/-) and PTX3(-/-) mice.

Main Results:

  • KpOmpA activates macrophages and DCs in a TLR2-dependent manner.
  • KpOmpA binds to scavenger receptors LOX-1 and SREC-I, independent of TLR2.
  • LOX-1 cooperates with TLR2 to trigger cellular responses.
  • TLR2 activation leads to the production of the long pentraxin PTX3.
  • PTX3 binds KpOmpA and amplifies the innate immune response.
  • In vivo inflammation induced by KpOmpA is dependent on TLR2 and PTX3.

Conclusions:

  • Scavenger receptor-mediated recognition of KpOmpA, coupled with TLR2-dependent activation, initiates a PTX3-mediated amplification loop in innate immunity.
  • This pathway is crucial for effective host defense against K. pneumoniae.
  • The findings reveal a novel mechanism of innate immune activation involving SRs, TLR2, and PTX3.

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