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A protein secreted by the respiratory pathogen Chlamydia pneumoniae impairs IL-17 signalling via interaction with

Katerina Wolf1, Gregory V Plano, Kenneth A Fields

  • 1Department of Microbiology and Immunology, University of Miami Miller School of Medicine, Miami, FL 33101, USA.

Cellular Microbiology
|January 23, 2009
PubMed

Insights

Chlamydia pneumoniae uses a novel protein, CP0236, to interact with host cell activator 1 (Act1). This interaction inhibits NFκB activation, protecting infected cells from inflammatory responses.

Area of Science:

  • Microbiology
  • Cell Biology
  • Immunology

Background:

  • Chlamydia pneumoniae is an obligate intracellular parasite causing respiratory infections and linked to chronic diseases.
  • Chlamydial inclusions are key sites for host-pathogen interaction, mediated by inclusion membrane proteins.
  • NFκB activation is a critical inflammatory pathway often dysregulated in chronic inflammatory conditions.

Purpose of the Study:

  • To identify and characterize novel Chlamydia pneumoniae inclusion membrane proteins involved in host cell manipulation.
  • To investigate the interaction between C. pneumoniae CP0236 and host cell proteins.
  • To elucidate the role of this interaction in modulating host inflammatory signaling pathways, specifically NFκB activation.

Main Methods:

  • Yeast two-hybrid screening to identify interacting partners of CP0236.
  • Co-immunoprecipitation assays in HeLa 229 cells to confirm protein-protein interactions.
  • Confocal microscopy to visualize the subcellular localization of Act1 in infected cells.
  • Stimulation assays with IL-17A to assess NFκB activation and pathway inhibition.

Main Results:

  • A novel C. pneumoniae inclusion membrane protein, CP0236, was identified.
  • CP0236 interacts with the NFκB activator 1 (Act1) in yeast and human cells.
  • C. pneumoniae infection causes Act1 to associate with the chlamydial inclusion membrane.
  • This sequestration of Act1 by chlamydiae inhibits IL-17 receptor signaling and subsequent NFκB activation.

Conclusions:

  • Chlamydia pneumoniae employs a unique mechanism to evade host immune responses by targeting Act1 via CP0236.
  • The interaction between CP0236 and Act1 disrupts the IL-17 signaling pathway, leading to suppressed NFκB activation.
  • This study reveals a novel host immune evasion strategy by C. pneumoniae, offering potential therapeutic targets.

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