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MAPK-PPARα/γ signal transduction pathways are involved in Chlamydia pneumoniae-induced macrophage-derived foam cell

Bei Cheng1, Xiaohua Wu1, Shan Sun1

  • 1Department of Gerontology, Union Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan 430022, China.

Microbial Pathogenesis
|March 25, 2014
PubMed

Insights

Chlamydia pneumoniae infection promotes atherosclerosis by increasing foam cell formation. This involves Mitogen-activated protein kinase (MAPK) and peroxisome proliferator-activated receptors (PPARs) signaling pathways.

Area of Science:

  • Cardiovascular Research
  • Infectious Diseases
  • Cell Biology

Background:

  • Chlamydia pneumoniae (C. pneumoniae) is a recognized risk factor for atherosclerosis.
  • Foam cell formation is a key process in the development of atherosclerotic plaques.

Purpose of the Study:

  • To investigate the role of MAPK and PPAR signaling pathways in C. pneumoniae-induced foam cell formation.
  • To elucidate the molecular mechanisms linking C. pneumoniae infection to atherogenesis.

Main Methods:

  • Utilized THP-1 macrophages treated with LDL and infected with C. pneumoniae.
  • Employed specific inhibitors and agonists for MAPK (JNK1/2, ERK1/2, p38) and PPAR (PPARγ, PPARα) pathways.
  • Assessed lipid accumulation, foam cell formation, and protein/mRNA expression levels.

Main Results:

  • C. pneumoniae infection significantly increased foam cell formation and lipid accumulation in macrophages.
  • Inhibition of JNK1/2 and ERK1/2, but not p38, reduced C. pneumoniae-induced lipid accumulation.
  • C. pneumoniae infection downregulated PPARγ and PPARα expression and activated MAPK signaling.
  • PPAR agonists reversed MAPK activation, while PPAR antagonists enhanced it.
  • JNK1/2 and ERK1/2 inhibition prevented C. pneumoniae-induced PPAR downregulation.

Conclusions:

  • MAPK-PPARα/γ reciprocal signaling pathways are critically involved in C. pneumoniae-induced foam cell formation.
  • This interaction contributes to the facilitation of atherogenesis by C. pneumoniae infection.
Keywords:
AtherosclerosisChlamydia pneumoniaeFoam cellsMitogen-activated protein kinasePeroxisome proliferator-activated receptors

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