Nonsteroidal antiinflammatory agents inhibit upregulation of CD11b, CD11c, and CD35 in neutrophils stimulated by formyl-methionine-leucine-phenylalanine.
Nonsteroidal antiinflammatory agents inhibit upregulation of CD11b, CD11c, and CD35 in neutrophils stimulated by formyl-methionine-leucine-phenylalanine.
复制标题
非甾体类抗炎药可抑制甲酰甲硫氨酸-亮氨酸-苯丙氨酸刺激的中性粒细胞中 CD11b、CD11c 和 CD35 的上调。
DOI：
10.1007/bf00917455
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发表时间：
1990
期刊：
影响因子：
5.1
通讯作者：
VanEpps,DE
中科院分区：
文献类型：
--
作者：
Crowell,RE;VanEpps,DE
非甾体类抗炎药（NSAIDs）抑制合成甲酰肽刺激的PMN聚集、趋化性、脱粒和超氧阴离子产生。这些功能中的许多依赖于补体成分C3b和iC3b的受体（分别为CD35和CD11b）或粘附分子CD11b和CD11c。使用流式细胞术和特异性单克隆抗体，我们研究了非甾体抗炎药吡罗昔康和吲哚美辛对FMLP，C5a或离子霉素刺激的PMN上这些细胞表面蛋白的上调的影响。在37 °C下孵育PMN增加了所有三种表面蛋白的表达。用FMLP、C5a或离子霉素刺激诱导进一步增加。吡罗昔康和吲哚美辛均抑制FMLP诱导的CD 11b、CD 1le和CD 35的上调，但两种药物均不影响C5a或离子霉素诱导的这些表面分子的上调。此外，吡罗昔康对37° C诱导的任何表面蛋白的上调没有影响，而吲哚美辛对37° C诱导的CD 11b上调没有影响，但抑制CD 11c和CD 35上调。FMLP对表面蛋白上调的抑制不是由于FMLP与PMNs结合的抑制。我们的结论是，吡罗昔康和吲哚美辛抑制FMLP受体介导的CD 11b，CD 11c，和CD 35在中性粒细胞的上调，但对这些分子的上调离子霉素或C5a没有影响。这些数据表明，吡罗昔康和吲哚美辛干扰FMLP刺激PMN的受体后信号事件。
Nonsteroidal antiinflammatory drugs (NSAIDs) inhibit PMN aggregation, chemotaxis, degranulation, and superoxide anion production stimulated by synthetic formyl peptides. Many of these functions are dependent upon receptors for the complement components C3b and iC3b (CD35 and CD11b, respectively), or the adherence molecules CD11b and CD11c. Using flow cytometry and specific monoclonal antibodies, we studied the effects of the NSAID piroxicam and indomethacin on the upregulation of these cell surface proteins on PMNs stimulated with FMLP, C5a, or ionomycin. Incubation of PMNs at 37 °C increased the expression of all three of these surface proteins. A further increase was induced by stimulation with FMLP, C5a, or ionomycin. Both piroxicam and indomethacin inhibited FMLP-induced upregulation of CD11b, CD1 le, and CD35, but neither drug affected the upregulation of these surface molecules induced by C5a or ionomycin. Furthermore, piroxicam had no effect on 37°C-induced upregulation of any of the surface proteins, while indomethacin showed no effect on 37°C-induced CD11b upregulation but suppressed CD11c and CD35 upregulation. Inhibition of surface protein upregulation by FMLP was not due to inhibition of FMLP binding to PMNs. We conclude that piroxicam and indomethacin inhibit FMLP receptor-mediated upregulation of CD 11b, CD11c, and CD35 in PMNs, but have no effect on the upregulation of these molecules by ionomycin or C5a. These data suggest that piroxicam and indomethacin interfere with postreceptor signaling events specific to PMN stimulation by FMLP.