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Peptidoglycan enhances secretion of monocyte chemoattractants via multiple signaling pathways

Sae-A Lee1, Sun-Mi Kim, Yong-Hae Son

  • 1Department of Pharmacology, School of Medicine, Pusan National University, Yangsan 626-870, Republic of Korea.

Biochemical and Biophysical Research Communications
|April 6, 2011
PubMed

Insights

Bacterial peptidoglycan (PG) promotes vascular inflammation in atherosclerosis by increasing mononuclear cell chemoattractants. This occurs via Toll-like receptor-2 (TLR-2) and downstream signaling pathways, contributing to artery disease progression.

Area of Science:

  • Immunology
  • Cardiovascular Biology
  • Microbiology

Background:

  • Peptidoglycan (PG) is prevalent in human atheromatous plaques, suggesting a role in vascular inflammation.
  • Understanding the molecular mechanisms of inflammatory responses to bacterial components in arteries is crucial.

Purpose of the Study:

  • To investigate the cellular factors mediating peptidoglycan-induced chemokine expression in mononuclear cells.
  • To elucidate the molecular pathways involved in bacterial pattern recognition in diseased arteries.

Main Methods:

  • Exposure of human monocytic leukemia THP-1 cells to peptidoglycan.
  • Analysis of chemokine (CCL2, CCL4) gene transcripts and secretion.
  • Inhibition studies using Toll-like receptor (TLR) antagonists and pathway-specific inhibitors (e.g., for Akt, MAPKs, PKC).

Main Results:

  • Peptidoglycan significantly enhanced CCL2 and CCL4 secretion and gene expression in THP-1 cells.
  • These effects were blocked by a TLR-2/4 inhibitor but not polymyxin B.
  • Peptidoglycan activated Akt, MAPKs, and protein kinase C, and pathway inhibitors attenuated chemokine up-regulation.

Conclusions:

  • Peptidoglycan contributes to vascular inflammation in atherosclerosis.
  • This occurs through upregulation of mononuclear cell chemoattractants via TLR-2, protein kinase C, Akt, mTOR, and MAPKs signaling pathways.

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