Differential expression of the CB2 cannabinoid receptor by rodent macrophages and macrophage-like cells in relation to cell activation

被引:265
作者
Carlisle, SJ [1 ]
Marciano-Cabral, F [1 ]
Staab, A [1 ]
Ludwick, C [1 ]
Cabral, GA [1 ]
机构
[1] Virginia Commonwealth Univ, Med Coll Virginia, Dept Microbiol & Immunol, Richmond, VA 23298 USA
关键词
cannabinoid receptors; CB1; CB2; macrophage activation; murine macrophage-like cells; murine peritoneal macrophages; neonatal rat microglia;
D O I
10.1016/S1567-5769(01)00147-3
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
An in vitro model of multi-step activation, in which cells of macrophage lineage are driven sequentially through inflammatory, primed, and fully activated states, was employed to assess for cannabinoid receptor expression. Murine and rat peritoneal macrophages, murine RAW264.7 and P388D(1) macrophage-like cells, and neonatal rat brain cortex microglia expressed the cannabinoid receptor type 2 (CB2) differentially in relation to cell activation. The CB2 was undetectable in resident peritoneal macrophages, present at high levels in thioglycolate-elicited inflammatory and interferon gamma (IFN gamma)-primed peritoneal macrophages, and detected at significantly diminished levels in bacterial lipopolysaccharide (LPS)-activated peritoneal macrophages. A comparable pattern of differential expression of the CB2 was noted for murine macrophage-like cells and neonatal rat brain cortex microglia. The cannabinoid receptor type 1 (CB1) was not detected in peritoneal macrophages or murine macrophage-like cells regardless of cell activation state but was present in neonatal rat microglia at low levels. These results indicate that levels of the CB2 in cells of macrophage lineage undergo major modulatory changes in relation to cell activation. Furthermore, since inflammatory and primed macrophages express the highest levels of CB2, the functional activities of macrophages when in these respective states of activation may be the most sensitive to the action of cannabinoids. (C) 2002 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:69 / 82
页数:14
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