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Chlamydia pneumoniae modulates human monocyte-derived dendritic cells functions driving the induction of a Type

Davide Flego1, Manuela Bianco, Adriano Quattrini

  • 1Department of Infectious, Parasitic and Immune-Mediated Diseases, Istituto Superiore di Sanità, Viale Regina Elena 299, 00161 Rome, Italy.

Microbes and Infection
|November 21, 2012
PubMed

Insights

Chlamydia pneumoniae infection modulates dendritic cell (DC) function via Toll-like receptor 2 (TLR2) and ERK1/2 signaling. This pathway promotes a pro-inflammatory Type 1/Type 17 immune response, impacting chronic inflammatory diseases.

Area of Science:

  • Immunology
  • Microbiology
  • Cell Biology

Background:

  • Chlamydia pneumoniae is a respiratory pathogen linked to chronic inflammatory diseases.
  • Dendritic cells (DCs) are crucial for C. pneumoniae dissemination from the lungs.
  • The impact of C. pneumoniae on DC function requires further elucidation.

Purpose of the Study:

  • To investigate how C. pneumoniae infection modulates human monocyte-derived dendritic cell (MDDC) functions.
  • To identify the intracellular pathways involved in C. pneumoniae-induced DC responses.

Main Methods:

  • Human MDDCs were infected with C. pneumoniae.
  • Bacterial load, gene expression (CPn1046), and cytokine production (IL-12p70, IL-1β, IL-6, IL-10) were measured.
  • The roles of Toll-like receptor 2 (TLR2) and ERK1/2 signaling were assessed using specific inhibitors and antibodies.

Main Results:

  • C. pneumoniae infection increased bacterial counts and CPn1046 expression in MDDCs.
  • Infected MDDCs matured and produced pro-inflammatory cytokines, driving a Type 1/Type 17 T cell response.
  • TLR2 and ERK1/2 activation by C. pneumoniae were critical for this response; inhibiting them shifted polarization to Type 2.

Conclusions:

  • C. pneumoniae utilizes TLR2 and ERK1/2 pathways to manipulate DC function.
  • This manipulation promotes a Type 1/Type 17 pro-inflammatory response, contributing to C. pneumoniae-associated pathologies.
  • Understanding these mechanisms offers insights into host-pathogen interactions in respiratory infections.

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