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- Title
Acute inflammatory reactions caused by histamine via monocytes/macrophages chronically participate in the initiation and progression of atherosclerosis.
- Authors
Kimura, Satoshi; Wang, Ke-Yong; Tanimoto, Akihide; Murata, Yoshitaka; Nakashima, Yasuhide; Sasaguri, Yasuyuki
- Abstract
Previously we demonstrated that histidine decarboxylase (HDC), which produces histamine from l-histidine, was detected in monocytes/macrophages located in human atherosclerotic lesions. As monocytic migration is a key event of atherogenesis, we investigated whether histamine induces monocytic expression of monocyte chemoattractant protein (MCP)-1 and its receptors CCR2-A and -B, and also endothelial expression of ICAM-1 and VCAM-1. Furthermore, we studied the effect of interleukin (IL)-4, which inhibits the HDC expression, on the expression of MCP-1 and CCR2. Histamine stimulated monocytes, but not macrophages, to express MCP-1 and CCR2-A and -B. The expression of MCP-1 was inhibited by histamine H2 blocker. In contrast, IL-4 enhanced CCR2 expression but not MCP-1. Histamine stimulated endothelial cells to express ICAM-1 and VCAM-1. These results indicate that histamine and IL-4, which are both synthesized in the arterial intima, chronically participates in the pathogenesis of atherosclerosis via the enhanced expression of monocytic MCP-1, CCR2 and endothelial adhesion molecules.
- Subjects
ATHEROSCLEROSIS; HISTAMINE; INFLAMMATION; MONOCYTES; INTERLEUKINS
- Publication
Pathology International, 2004, Vol 54, Issue 7, p465
- ISSN
1320-5463
- Publication type
Article
- DOI
10.1111/j.1440-1827.2004.01653.x