PMID- 9195529
OWN - NLM
STAT- MEDLINE
DCOM- 19970812
LR  - 20071115
IS  - 0315-162X (Print)
IS  - 0315-162X (Linking)
VI  - 24
IP  - 6
DP  - 1997 Jun
TI  - Evidence for RANTES, monocyte chemotactic protein-1, and macrophage inflammatory 
      protein-1 beta expression in Kawasaki disease.
PG  - 1179-85
AB  - OBJECTIVE: Patients with Kawasaki disease mount an immune response directed to 
      their abnormally stimulated vascular endothelium, that is associated with 
      vascular inflammation and injury and a predisposition to arterial aneurysm 
      formation. This suggests that specific pro-inflammatory cytokines may mediate 
      these hyperreactive responses. The selective chemoattractant and activation 
      effects of chemokines on lymphocytes identifies them as potential candidates in 
      mediating selective inflammatory processes in Kawasaki disease. We examined 
      peripheral blood from patients with Kawasaki disease for chemokine gene 
      expression. METHODS: Consecutive samples from 14 patients during the acute, 
      subacute, and convalescent phases of their illness were collected and elaborated 
      for RANTES, macrophage inflammatory protein-1 beta (MIP-1 beta) and monocyte 
      chemotactic protein-1 (MCP-1) expression. RESULTS: RANTES and MCP-1 gene 
      expression levels were significantly elevated in 12 of the 14 patients, and MIP-1 
      beta gene expression was elevated in 13 of the 14 patients. There was no obvious 
      correlation between clinical phase of the disease and chemokine expression level, 
      yet elevated expression levels were detected in all phases, including the 
      convalescent phase, when laboratory evidence of lymphocyte activation has been 
      shown to return to normal. Serial samples showed persistence or increased 
      expression of chemokine genes into the convalescent phase in patients with 
      coronary artery lesions. CONCLUSION: Chemokine mediated inflammatory events may 
      persist in the convalescent phase of Kawasaki disease and may contribute to 
      further risk of vascular endothelial cell injury, specifically coronary aneurysm 
      formation.
FAU - Wong, M
AU  - Wong M
AD  - Department of Medical Genetics and Microbiology, Faculty of Medicine, University 
      of Toronto, Canada.
FAU - Silverman, E D
AU  - Silverman ED
FAU - Fish, E N
AU  - Fish EN
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Canada
TA  - J Rheumatol
JT  - The Journal of rheumatology
JID - 7501984
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CCL4)
RN  - 0 (Chemokine CCL5)
RN  - 0 (Chemokines)
RN  - 0 (Macrophage Inflammatory Proteins)
RN  - 0 (RNA, Messenger)
SB  - IM
MH  - Chemokine CCL2/genetics/*metabolism
MH  - Chemokine CCL4
MH  - Chemokine CCL5/genetics/*metabolism
MH  - Chemokines/genetics/*metabolism
MH  - Child
MH  - Child, Preschool
MH  - Humans
MH  - Infant
MH  - Macrophage Inflammatory Proteins/genetics/*metabolism
MH  - Mucocutaneous Lymph Node Syndrome/*metabolism
MH  - Polymerase Chain Reaction
MH  - RNA, Messenger/metabolism
EDAT- 1997/06/01 00:00
MHDA- 1997/06/01 00:01
CRDT- 1997/06/01 00:00
PHST- 1997/06/01 00:00 [pubmed]
PHST- 1997/06/01 00:01 [medline]
PHST- 1997/06/01 00:00 [entrez]
PST - ppublish
SO  - J Rheumatol. 1997 Jun;24(6):1179-85.