NSAIDs upregulate beta(2)-integrin expression on human neutrophils through a calcium-dependent pathway

被引：22

作者：

Fiorucci, S

Santucci, L

Gerli, R

Brunori, PM

Federici, B

Ugolini, B

Fabbri, C

Morelli, A

机构：

[1] UNIV PERUGIA,DIPARTIMENTO MED CLIN,SERV GASTROENTEROL & ENDOSCOPIA DIGEST,I-06100 PERUGIA,ITALY

[2] UNIV PERUGIA,DIPARTIMENTO PATOL & FARMACOL,SERV GASTROENTEROL & ENDOSCOPIA DIGEST,I-06100 PERUGIA,ITALY

[3] UNIV PERUGIA,IST CLIN MED & SCI ONCOL 1,I-06100 PERUGIA,ITALY

[4] UNIV PERUGIA,DIPARTIMENTO CHIRURG & EMERGENCE CHIRURG,I-06100 PERUGIA,ITALY

来源：

ALIMENTARY PHARMACOLOGY & THERAPEUTICS | 1997年 / 11卷 / 03期

关键词：

D O I：

10.1046/j.1365-2036.1997.00190.x

中图分类号：

R57 [消化系及腹部疾病];

学科分类号：

摘要：

Background: Margination of circulating neutrophils (PMN) into the gastric microcirculation is an early and critical event in the pathogenesis of non-steroidal antinflammatory drug (NSAID)-induced gastropathy. This effect is mediated through the upregulation of beta(2) integrins on the PMN surface. Aims: To investigate whether indomethacin modulates: (1) Mac-1 expression; (2) Ca2+ mobilization ([Ca2+](i)), protein kinase C and nitric oxide accumulation; and (3) mitogen-associated protein kinase phosphorylation in human PMN. Methods: Human PMN were isolated by centrifugation through a double Ficoll gradient. [Ca2+](i) was measured in PMN loaded with fura-2 and Mac-1 expression by flow cytometry. Results: Indomethacin caused a concentration- and time-dependent upregulation of CD11b and CD18 expression and PMN adhesion to endothelial cells, Maximal upregulation of Mac-1 expression (40-50%) occurred after a 30-min incubation with 0.1 mM.

引用

页码：619 / 630

页数：12

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[1] NONSTEROIDAL ANTIINFLAMMATORY DRUGS EXERT DIFFERENTIAL-EFFECTS ON NEUTROPHIL FUNCTION AND PLASMA-MEMBRANE VISCOSITY - STUDIES IN HUMAN NEUTROPHILS AND LIPOSOMES [J].