IL-10 up-regulates nitric oxide (NO) synthesis by lipopolysaccharide (LPS)-activated macrophages:: improved control of Trypanosoma cruzi infection

被引:36
|
作者
Jacobs, F
Chaussabel, D
Truyens, C
Leclerq, V
Carlier, Y
Goldman, M
Vray, B
机构
[1] Free Univ Brussels, Fac Med, Expt Immunol Lab, Brussels, Belgium
[2] Free Univ Brussels, Fac Med, Parasitol Lab, Brussels, Belgium
来源
CLINICAL AND EXPERIMENTAL IMMUNOLOGY | 1998年 / 113卷 / 01期
关键词
IL-10; Trypanosoma cruzi; nitric oxide; lipopolysaccharide; macrophages;
D O I
10.1046/j.1365-2249.1998.00637.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
We examined the effects of IL-10 on tumour necrosis factor-alpha (TNF-alpha) and NO production by LPS-activated macrophages and on the ability of these cells to control Trypanosoma cruzi infection. We first observed that the addition of rIL-10 to macrophages of the J774 cell line decreased their synthesis of TNF-alpha but increased their release of NO in a dose-dependent manner. In parallel, treatment of J774 cells with rIL-10 resulted in a better control of T. cruzi infection involving up-regulation of NO synthesis, as it was not observed in presence of N-nitro-L-arginine methyl ester (L-NAME), a competitive inhibitor of NO synthase. The enhancing effect of rIL-10 on NO production was not observed on peritoneal macrophages from wild-type C57B1/6 mice, but well on macrophages from IL-10 knock-out mice. The control of NO production by endogenous IL-10 was confirmed by the demonstration that neutralization of IL-10 secreted by LPS-activated macrophages from wild-type mice inhibited their production of NO and, in parallel, their ability to control T. cruzi infection. Taken together, these data demonstrate that both exogenous and endogenous IL-10 up-regulate the production of NO by LPS-activated macrophages and improve thereby their ability to clear T. cruzi infection.
引用
收藏
页码:59 / 64
页数:6
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