Induction of human macrophage vascular endothelial growth factor and intercellular adhesion molecule-1 by Ureaplasma urealyticum and downregulation by steroids

被引:17
作者
Li, YH [1 ]
Brauner, A
Jensen, JS
Tullus, K
机构
[1] Karolinska Inst, Neonatal Unit, Astrid Lindgren Childrens Hosp, SE-17176 Stockholm, Sweden
[2] Karolinska Hosp, Dept Clin Microbiol, S-10401 Stockholm, Sweden
[3] State Serum Inst, Copenhagen, Denmark
来源
BIOLOGY OF THE NEONATE | 2002年 / 82卷 / 01期
关键词
Ureaplasma urealyticum; chronic lung disease; macrophages; vascular endothelial growth factor; intercellular adhesion molecule-1;
D O I
10.1159/000064148
中图分类号
R72 [儿科学];
学科分类号
100202 ;
摘要
Chronic lung disease (CLD) remains a major cause of morbidity for the prematurely born infant. The pathogenesis of CLD is complex and has not been defined entirely. Infection and lung inflammatory events have been thought to play a key role in the development of CLD. However, the contribution of Ureaplasma urealyticum to the development of CLD is debated and steroids produce some improvement in neonates with this disease. The aim of this study was to investigate if U. urealyticum could stimulate macrophages to produce vascular endothelial growth factor (VEGF) and intercellular adhesion molecule-1 (ICAM-1) in vitro, which are potentially associated with both early and later pathological changes in the lung during the development of CLD. In addition, the impact of dexamethasone and budesonide on these processes was examined. We found that U. urealyticum antigen (greater than or equal to4 x 10(7) color-changing units/ml) stimulated human macrophages (phorbol 12-myristate 13-acetate-differentiated THP-1 cell line) to produce VEGF and soluble ICAM-1 in a dose-dependent manner (p < 0.05) measured by ELISA. Likewise, cell surface ICAM-1 (CD54) measured by flow cytometry was increased after stimulation with U. urealyticum. This effect was attenuated by budesonide and clexamethasone (p < 0.05). The mRNA expressions of VEGF and ICAM-1 detected by a semiquantitative reverse transcriptase polymerase chain reaction were also induced in response to U. urealyticum and inhibited by the steroids (p < 0.05). The expression of ICAM-1 was reduced by 85.5% when the TNF-alpha production was neutralized with an anti-TNF-alpha antibody. Our findings imply that U. urealyticum might be involved in the development of CLD of prematurity. Copyright (C) 2002 S. KargerAG, Basel.
引用
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页码:22 / 28
页数:7
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