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Rapid and Robust Analysis of Cellular and Molecular Polarization Induced by Chemokine Signaling
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C-reactive protein promotes monocyte chemoattractant protein-1--mediated chemotaxis through upregulating CC chemokine

Ki Hoon Han1, Kyung-Hee Hong, Jae-Hyeong Park

  • 1Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea. steadyhan@amc.seoul.kr

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|May 12, 2004
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C-reactive protein (CRP) directly activates human monocytes, increasing their migration. This suggests elevated CRP may drive monocyte accumulation in arteries, promoting atherosclerosis.

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Area of Science:

  • Cardiovascular Science
  • Immunology
  • Molecular Biology

Background:

  • Inflammation is central to atherosclerosis development.
  • Elevated C-reactive protein (CRP) predicts cardiovascular events and may promote atherogenesis.
  • The direct role of CRP in human monocyte activation requires further investigation.

Purpose of the Study:

  • To determine if C-reactive protein (CRP) directly activates human circulating monocytes.
  • To elucidate the mechanisms underlying CRP-mediated monocyte activation.
  • To correlate in vivo CRP levels with monocyte activation markers.

Main Methods:

  • THP-1 monocytes were incubated with CRP to assess CC chemokine receptor 2 (CCR2) expression and chemotaxis.
  • Fcgamma receptor (FcgammaR) involvement and phospholipase D1 activation were investigated.
  • Serum high-sensitivity CRP levels were correlated with monocyte CCR2 expression and chemotaxis in human subjects.

Main Results:

  • CRP (10 microg/mL) significantly increased CCR2 expression and monocyte chemoattractant protein-1 (MCP-1)-mediated chemotaxis.
  • CRP-induced CCR2 upregulation involved FcgammaRI binding and phospholipase D1 activation.
  • In vivo, higher serum CRP levels correlated with increased monocyte CCR2 expression and MCP-1-mediated chemotaxis.

Conclusions:

  • Elevated C-reactive protein (CRP) directly enhances monocyte chemotactic activity.
  • CRP may promote monocyte recruitment into the arterial wall, contributing to atherogenesis.
  • These findings highlight a direct mechanistic link between CRP and the inflammatory processes in atherosclerosis.