肿瘤坏死因子α对白细胞黏附分子上调的抑制作用：柳氮磺胺吡啶的一种新作用机制。
Inhibition of leucocyte adhesion molecule upregulation by tumor necrosis factor alpha: a novel mechanism of action of sulphasalazine.
作者信息
Greenfield S M, Hamblin A S, Shakoor Z S, Teare J P, Punchard N A, Thompson R P
机构信息
Gastrointestinal Laboratory, Rayne Institute, St Thomas' Hospital, London.
出版信息
Gut. 1993 Feb;34(2):252-6. doi: 10.1136/gut.34.2.252.
Abstract
The effects of the cytokine tumour necrosis factor alpha and the calcium ionophore A23187 upon CD11a, CD11b, CD11c and CD18 leucocyte membrane expression was analysed in whole blood using monoclonal antibodies and flow cytometry. Both agents significantly increased the density of CD11b/CD18 membrane expression on monocytes and granulocytes, but had no effects on adhesion molecule expression on lymphocytes. The effects of sulphasalazine, 5-aminosalicylic acid (5-ASA) and sulphapyridine upon adhesion molecule upregulation were then examined; 10(-3) and 10(-4) M sulphasalazine and 5-ASA significantly reduced tumour necrosis factor alpha induced CD11b/CD18 upregulation on monocytes and granulocytes but had no effects upon A23187 mediated upregulation. Sulphapyridine was inactive. These results suggest that sulphasalazine and 5-ASA may interfere with mechanisms of leucocyte recruitment in inflammatory bowel disease.
摘要
利用单克隆抗体和流式细胞术，在全血中分析了细胞因子肿瘤坏死因子α和钙离子载体A23187对CD11a、CD11b、CD11c和CD18白细胞膜表达的影响。这两种试剂均显著增加了单核细胞和粒细胞上CD11b/CD18膜表达的密度，但对淋巴细胞上粘附分子的表达没有影响。随后研究了柳氮磺胺吡啶、5-氨基水杨酸（5-ASA）和磺胺吡啶对粘附分子上调的影响；10⁻³和10⁻⁴M的柳氮磺胺吡啶和5-ASA显著降低了肿瘤坏死因子α诱导的单核细胞和粒细胞上CD11b/CD18的上调，但对A23187介导的上调没有影响。磺胺吡啶没有活性。这些结果表明，柳氮磺胺吡啶和5-ASA可能会干扰炎症性肠病中白细胞募集的机制。
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