Regulation of ICAM-1 expression in mouse macrophages
Regulation of ICAM-1 expression in mouse macrophages
复制标题
DOI：
10.1023/a:1007029409521
复制
发表时间：
2000-04-01
期刊：
影响因子：
5.1
通讯作者：
Giardina, C
中科院分区：
文献类型：
--
作者：
Hubbard, AK;Giardina, C
在二氧化硅（SI）诱导的肺损伤的小鼠模型中，SI暴露增加肺（肺泡/间质）巨噬细胞和肺泡II型上皮细胞上的细胞间粘附分子-1（ICAM-1）的表达。为了研究SI诱导的小鼠巨噬细胞ICAM-1表达的调节，评价了由颗粒二氧化硅（α石英; 20 μ g/ml; 6 μ g/cm（2））或炎性细胞因子TNF α（20 ng/ml）诱导的新鲜分离的巨噬细胞（肺泡、腹膜）和巨噬细胞系（MH-S，RAW 264.7）的ICAM-1表达。TNF α显著增加了所有细胞类型中ICAM-1的表达，而SI引起了腹膜巨噬细胞（PM）和细胞系MH-S的增加。免疫细胞化学证实了这种表达增加的模式。为了研究ICAM-1表达的调节，将PM与SI、TNF α或与抗TNF α抗体、抗氧化剂NAG或iNOS合成酶抑制剂L-NAME伴随的培养基一起孵育。抗TNF α和NAG，但不是L-NAME，抑制诱导（TNF α，SI）以及组成（媒体）ICAM-1的表达。这些数据表明，炎性细胞因子和无机颗粒都可以增加小鼠巨噬细胞上的ICAM-1表达，并且这种表达部分由TNF α和活性氧介导。
In a mouse model of silica (SI) induced Lung injury, SI exposure increases expression of intercellular adhesion molecule-1 (ICAM-1) on lung (alveolar/interstitial) macrophages and alveolar type II epithelial cells. To investigate the regulation of SI induced ICAM-1 expression on mouse macrophages, freshly isolated macrophages (alveolar, peritoneal) and macrophage cell lines (MH-S, RAW 264.7) were evaluated for ICAM-1 expression elicited by the particle silica (alpha quartz; 20 mu g/ml; 6 mu g/cm(2)) or the inflammatory cytokine, TNF alpha (20 ng/ml). TNF alpha significantly increased ICAM-1 expression in all cell types whereas SI elicited an increase in peritoneal macrophages (PM) and the cell line, MH-S. This pattern of increased expression was confirmed by immunocytochemistry. To investigate the regulation of ICAM-1 expression, PM were incubated with SI, TNF alpha or media concomitantly with anti-TNF alpha antibody, the antioxidant, NAG, or the iNOS synthase inhibitor, L-NAME. Both anti-TNF alpha and NAG, but not L-NAME, inhibited elicited (TNF alpha, SI) as well as constitutive (media) ICAM-1 expression. These data demonstrate that both inflammatory cytokines and inorganic particles can increase ICAM-1 expression on mouse macrophages and that this expression is mediated, in part, by TNF alpha and reactive oxygen species.