Serum amyloid A-induced mRNA expression and release of tumor necrosis factor-alpha (TNF-α) in human neutrophils

被引：51

作者：

Hatanaka, E ^{[1
]}

Furlaneto, CJ

Ribeiro, FP

Souza, GM

Campa, A

机构：

[1] Univ Sao Paulo, Fac Ciencias Farmaceut, Dept Anal Clin & Toxicol, BR-05508900 Sao Paulo, Brazil

[2] Univ Sao Paulo, Inst Quim, Dept Bioquim, BR-01498 Sao Paulo, Brazil

来源：

IMMUNOLOGY LETTERS | 2004年 / 91卷 / 01期

基金：

巴西圣保罗研究基金会;

关键词：

atherosclerosis; cancer; serum amyloid A; inflammation; TNF-alpha;

D O I：

10.1016/j.imlet.2003.09.011

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Recently, we described the effect of the acute phase protein serum amyloid A (SAA) on the mRNA expression and release of IL-8 in neutrophils [Mediators Inflamm. 12 (3) (2003) 173]. Here, we expand this earlier study, focusing on tumor necrosis factor-alpha (TNF-alpha) m-RNA expression and protein release. Our findings indicate that SAA stimulates the rapid expression and release of TNF-alpha from cultured human blood neutrophils. The release of TNF-alpha from SAA-stimulated neutrophils is strongly suppressed by the addition of the antioxidants N-acetyl-L-cysteine, alpha-mercaptoethanol, glutathione, the antiinflammatory dexamethasone and the compounds wortmannin (a PI3K inhibitor), PD98059 (a MEK-1 inhibitor) and SB203580 (a p38 inhibitor). Monocytes also responded to SAA by releasing TNF-alpha. These data are congruent with the increasing evidence of the role of SAA in modulating inflammatory and immune responses, possibly contributing to the pool of cytokines produced in acute inflammation and in chronic diseases. (C) 2003 Elsevier B.V. All rights reserved.

引用

页码：33 / 37

页数：5

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