INHIBITION OF LEUKOCYTE ADHESION MOLECULE UP-REGULATION BY TUMOR-NECROSIS-FACTOR-ALPHA - A NOVEL MECHANISM OF ACTION OF SULFASALAZINE

被引：49

作者：

GREENFIELD, SM ^{[1
]}

HAMBLIN, AS ^{[1
]}

SHAKOOR, ZS ^{[1
]}

TEARE, JP ^{[1
]}

PUNCHARD, NA ^{[1
]}

THOMPSON, RPH ^{[1
]}

机构：

[1] ST THOMAS HOSP,DEPT IMMUNOL,LONDON SE1 7EH,ENGLAND

来源：

GUT | 1993年 / 34卷 / 02期

关键词：

D O I：

10.1136/gut.34.2.252

中图分类号：

R57 [消化系及腹部疾病];

学科分类号：

摘要：

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.

引用

页码：252 / 256

页数：5

共 29 条

[1] INCREASED EXPRESSION OF AN ADHESION-PROMOTING SURFACE GLYCOPROTEIN IN THE GRANULOCYTOPENIA OF HEMODIALYSIS [J].