RCMV increases intimal hyperplasia by inducing inflammation, MCP-1 expression and recruitment of adventitial cells to

Monika K Grudzinska1, Krzysztof Bojakowski2, Joanna Soin3

  • 1Experimental Cardiovascular Research Unit, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden.

Herpesviridae
|March 25, 2011
PubMed
Abstract

Insights

Rat cytomegalovirus (CMV) infection accelerates transplant vasculopathy by increasing macrophage infiltration and inflammation. This leads to adventitial cell recruitment and heightened intimal hyperplasia in allografts.

Area of Science:

  • Vascular Biology
  • Transplantation Immunology
  • Virology

Background:

  • Cytomegalovirus (CMV) infection is linked to accelerated transplant vasculopathy.
  • This study investigates the impact of acute rat CMV (RCMV) infection on vessel remodeling in transplant vasculopathy.

Purpose of the Study:

  • To assess the effects of RCMV infection on allograft morphology, inflammation, and adventitial cell contribution to intimal hyperplasia.

Main Methods:

  • Rats underwent infrarenal aorta transplantation with local RCMV infection.
  • Graft analysis included intimal hyperplasia, collagen degradation, and inflammation at 2 and 8 weeks.
  • Adventitial cell migration to the intima was studied using labeled isogenic adventitia.

Main Results:

  • RCMV infection increased intimal hyperplasia threefold in allografts.
  • RCMV induced medial apoptosis, matrix metalloproteinase 2 expression, and reduced collagen.
  • Macrophage infiltration and MCP-1 production increased, with RCMV-infected macrophages found in adventitia and intima.

Conclusions:

  • RCMV infection enhances macrophage infiltration and MCP-1 production, promoting inflammation.
  • This process recruits adventitial cells to the intima, accelerating intimal hyperplasia.
  • RCMV significantly contributes to the pathogenesis of transplant vasculopathy.

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