Cytokine-induced phagocyte adhesion to human mesangial cells: role of CD11/CD18 integrins and ICAM-1.
Cytokine-induced phagocyte adhesion to human mesangial cells: role of CD11/CD18 integrins and ICAM-1.
复制标题
细胞因子诱导的吞噬细胞粘附到人系膜细胞：CD11/CD18 整合素和 ICAM-1 的作用。
DOI：
10.1152/ajprenal.1991.261.6.f1071
复制
发表时间：
1991
期刊：
影响因子：
--
通讯作者：
Brady,HR
中科院分区：
文献类型：
--
作者：
Denton,MD;Marsden,PA;Luscinskas,FW;Brenner,BM;Brady,HR
我们检测了肿瘤坏死因子- α (tnf - α)和白细胞介素-1 β (IL-1 β)对中性粒细胞和单核细胞（吞噬细胞）粘附人系膜细胞单层（HMC）的作用，并利用亚单位特异性单克隆抗体（MAb）评估了吞噬细胞CD11/CD18整合素粘附分子和HMC细胞间粘附分子-1 （ICAM-1）在这一过程中的作用。TNF，而不是IL-1，通过吞噬细胞导向的作用，引起了中性粒细胞和单核细胞对HMC的快速（发病时间小于1分钟）粘附。针对CD18和CD11b的单抗可显著抑制粘附，而针对CD11a、CD11c或ICAM-1的单抗作用较弱或无抑制作用。相反，HMC长时间暴露于TNF或IL-1 （1-18 h）会增加HMC对吞噬细胞的粘附性。这些作用被放线菌素D或环己亚胺以及针对HMC ICAM-1或吞噬细胞CD18、CD11a或CD11b的单抗阻断，表明细胞因子通过诱导HMC ICAM-1合成而引起粘附。与这一解释一致的是，通过间接免疫荧光测定，TNF治疗HMC与ICAM-1表面表达增加有关，通过Northern blot分析，与ICAM-1 mRNA水平增加有关。TNF对吞噬细胞和HMC的作用是加性的。通过51Cr释放确定的HMC损伤仅在吞噬细胞和HMC均被TNF激活时观察到。抗cd18单抗和超氧化物歧化酶可减轻HMC损伤，表明损伤过程在一定程度上依赖于粘附并由活性氧介导。（摘要删节250字）
We examined the actions of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta) on neutrophil and monocyte (phagocyte) adhesion to human mesangial cell monolayers (HMC) and assessed the role of phagocyte CD11/CD18 integrin adhesion molecules and HMC intercellular adhesion molecule-1 (ICAM-1) in this process, using subunit specific monoclonal antibodies (MAb). TNF, but not IL-1, provoked rapid (onset less than 1 min) neutrophil and monocyte adhesion to HMC by a phagocyte-directed action. Adhesion was markedly inhibited by MAb against CD18 and CD11b, with lesser or no inhibition being afforded by MAb against CD11a, CD11c, or ICAM-1. In contrast, prolonged exposure of HMC to TNF or IL-1 (1-18 h) increased HMC adhesiveness for phagocytes. These actions were blocked by actinomycin D or cycloheximide and by MAb against HMC ICAM-1 or phagocyte CD18, CD11a, or CD11b, suggesting that cytokines provoked adhesion by inducing HMC ICAM-1 synthesis. In keeping with this interpretation, TNF treatment of HMC was associated with increased ICAM-1 surface expression, as determined by indirect immunofluorescence, and increased ICAM-1 mRNA levels, as determined by Northern blot analysis. The actions of TNF on phagocytes and HMC were additive. HMC injury, as determined by 51Cr release, was only observed when both phagocytes and HMC were activated by TNF. HMC injury was attenuated by anti-CD18 MAb and superoxide dismutase, suggesting that the injury process was, in part, adhesion dependent and mediated by reactive oxygen species.(ABSTRACT TRUNCATED AT 250 WORDS)