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Cox-2 inhibition abrogates Chlamydia pneumoniae-induced PGE2 and MMP-1 expression

Jan Rupp1, Mario Berger, Norbert Reiling

  • 1Institute of Medical Microbiology and Hygiene, University of Luebeck, Germany.

Biochemical and Biophysical Research Communications
|July 9, 2004
PubMed

Insights

Chlamydia pneumoniae infection in monocytes triggers vascular inflammation via cyclooxygenase-2 (Cox-2). Inhibiting Cox-2 may offer a new treatment for atherosclerosis linked to this persistent infection.

Area of Science:

  • Vascular Biology
  • Infectious Disease Immunology

Background:

  • Peripheral blood monocytes (PBMC) are implicated in vascular inflammation and atherosclerosis.
  • Chlamydia pneumoniae (Cp) infection of PBMC is prevalent in atherosclerotic patients and resistant to antibiotics, potentially causing vascular damage.

Purpose of the Study:

  • To investigate the role of cyclooxygenase-2 (Cox-2) in mediating proatherosclerotic mediators prostaglandin E2 (PGE2) and interstitial collagenase (MMP-1) in Cp-infected human PBMC.

Main Methods:

  • Analyzed Cox-2 mRNA and protein expression in Cp-infected human PBMC.
  • Investigated the involvement of p38 and p44/42 MAPkinases.
  • Assessed the effect of the selective Cox-2 inhibitor NS398 on PGE2 and MMP-1 synthesis.

Main Results:

  • Cp infection induced rapid and sustained Cox-2 expression, dependent on p38 and p44/42 MAPkinases.
  • Upregulation of PGE synthase and MMP-1 was abrogated by the Cox-2 inhibitor NS398.
  • Enhanced PGE2 and MMP-1 synthesis in Cp-infected PBMC is mediated by MAPK pathways and requires sustained Cox-2 activation.

Conclusions:

  • Cp infection activates a proatherosclerotic signaling cascade in PBMC involving Cox-2, p38, and p44/42 MAPkinases.
  • Selective Cox-2 inhibitors show potential as a therapeutic strategy for endovascular Cp infections contributing to atherosclerosis.

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