PMID- 11739289
OWN - NLM
STAT- MEDLINE
DCOM- 20020123
LR  - 20190706
IS  - 1524-4571 (Electronic)
IS  - 0009-7330 (Linking)
VI  - 89
IP  - 12
DP  - 2001 Dec 7
TI  - Cytomegalovirus infection accelerates inflammation in vascular tissue 
      overexpressing monocyte chemoattractant protein-1.
PG  - 1224-30
AB  - Cardiovascular disease is the leading cause of mortality in the United States. 
      Atherosclerosis is responsible for most of this pathology and is an inflammatory 
      disease with multiple cytokines and adhesion molecules expressed during 
      atherogenesis. Cytomegalovirus (CMV), monocytes, and monocyte chemoattractant 
      protein-1 (MCP-1) have all been implicated in human atherogenesis. A transgenic 
      mouse overexpressing MCP-1 in the myocardium and pulmonary arteries develops 
      myocarditis and pulmonary vascular inflammation. We infected MCP-1 transgenic 
      mice with a sublethal dose of murine cytomegalovirus (MCMV) to look for evidence 
      of accelerated inflammation in vascular tissues overexpressing MCP-1 to determine 
      if MCMV could interact with monocytes and MCP-1 in a manner similar to what may 
      occur in atherogenesis. MCMV infection of MCP-1 transgenic mice caused ascites, 
      myocarditis, and pulmonary artery inflammation, which was not present in 
      mock-infected MCP-1 or MCMV-infected wild-type mice. Inflammatory infiltrates in 
      these tissues consisted of macrophages and T lymphocytes similar to the 
      infiltrates seen in atherosclerosis. Virus presence in inflamed tissues was 
      demonstrated by infecting transgenic mice with MCMV recombinant virus containing 
      the gene sequence for the enhanced green fluorescent protein (EGFP). Human CMV 
      could be involved in atherogenesis in a similar manner by interacting with 
      monocytes and MCP-1 specifically expressed in vascular walls.
FAU - Froberg, M K
AU  - Froberg MK
AD  - Departments of Pathology, University of Minnesota-Duluth, School of Medicine, 
      Duluth, Minnesota, USA. kfroberg@d.umn.edu
FAU - Adams, A
AU  - Adams A
FAU - Seacotte, N
AU  - Seacotte N
FAU - Parker-Thornburg, J
AU  - Parker-Thornburg J
FAU - Kolattukudy, P
AU  - Kolattukudy P
LA  - eng
GR  - HL-48916/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Circ Res
JT  - Circulation research
JID - 0047103
RN  - 0 (Chemokine CCL2)
SB  - IM
MH  - Animals
MH  - Ascites/etiology/pathology
MH  - Body Weight
MH  - Chemokine CCL2/genetics/*metabolism
MH  - Cytomegalovirus/isolation & purification/pathogenicity
MH  - Cytomegalovirus Infections/complications/genetics/*metabolism/pathology
MH  - Disease Progression
MH  - Female
MH  - Genetic Predisposition to Disease
MH  - Immunohistochemistry
MH  - Liver/metabolism/pathology/virology
MH  - Lung/metabolism/pathology
MH  - Male
MH  - Mice
MH  - Mice, Transgenic
MH  - Monocytes/immunology/pathology
MH  - Myocarditis/genetics/*metabolism/pathology/virology
MH  - Myocardium/metabolism/pathology
MH  - Organ Size
MH  - Pulmonary Artery/*metabolism/pathology
MH  - Salivary Glands/virology
MH  - Spleen/metabolism/pathology/virology
MH  - T-Lymphocytes/immunology/pathology
MH  - Vasculitis/etiology/*metabolism/pathology
MH  - Viral Plaque Assay
EDAT- 2001/12/12 10:00
MHDA- 2002/01/24 10:01
CRDT- 2001/12/12 10:00
PHST- 2001/12/12 10:00 [pubmed]
PHST- 2002/01/24 10:01 [medline]
PHST- 2001/12/12 10:00 [entrez]
AID - 10.1161/hh2401.100601 [doi]
PST - ppublish
SO  - Circ Res. 2001 Dec 7;89(12):1224-30. doi: 10.1161/hh2401.100601.