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粒细胞巨噬细胞集落刺激因子、肿瘤坏死因子-α与小鼠巨噬细胞克氏锥虫感染之间的关系。

Relationship between granulocyte macrophage-colony stimulating factor, tumour necrosis factor-alpha and Trypanosoma cruzi infection of murine macrophages.

作者信息

Olivares Fontt E, Vray B

机构信息

Laboratoire d'Immunologie (CP 615), Faculté de Médecine, Université Libre de Bruxelles, Belgium.

出版信息

Parasite Immunol. 1995 Mar;17(3):135-41. doi: 10.1111/j.1365-3024.1995.tb01015.x.

DOI:10.1111/j.1365-3024.1995.tb01015.x
PMID:7792097
Abstract

Gamma interferon (IFN-gamma)-activated macrophages control Trypanosoma cruzi infection via nitric oxide (NO), recently recognized as a major effector molecule. Granulocyte macrophage-colony stimulating factor (GM-CSF) is a multipotent cytokine secreted by macrophages and many other cells. It induces the production of tumour necrosis factor alpha (TNF-alpha), another cytokine also secreted by macrophages and involved in the control of T. cruzi infection. However, no data are available on the relationship between GM-CSF, TNF-alpha and NO produced by macrophages activated by IFN-gamma and infected with T. cruzi. To highlight this relationship, mouse peritoneal macrophages (MPM) and two c-myc retrovirus-induced macrophage cell lines (9.1.1 and BMM8), respectively characterized by a constitutive and an inducible production of GM-CSF, were activated with IFN-gamma and/or GM-CSF and infected with T. cruzi. Our results indicate that T. cruzi upregulates GM-CSF release from MPM and from the two macrophage cell lines, activated (or not) by IFN-gamma. A high autocrine production of GM-CSF or an exogenous supply of GM-CSF is correlated with an enhanced release of TNF-alpha and NO, inducing an improved control of T. cruzi infection by IFN-gamma-activated MPM.

摘要

γ干扰素(IFN-γ)激活的巨噬细胞通过一氧化氮(NO)控制克氏锥虫感染,NO最近被认为是一种主要效应分子。粒细胞巨噬细胞集落刺激因子(GM-CSF)是一种由巨噬细胞和许多其他细胞分泌的多能细胞因子。它诱导肿瘤坏死因子α(TNF-α)的产生,TNF-α是另一种也由巨噬细胞分泌且参与控制克氏锥虫感染的细胞因子。然而,关于GM-CSF、TNF-α与被IFN-γ激活并感染克氏锥虫的巨噬细胞产生的NO之间的关系,目前尚无相关数据。为了阐明这种关系,分别以组成型和诱导型产生GM-CSF为特征的小鼠腹腔巨噬细胞(MPM)和两种c-myc逆转录病毒诱导的巨噬细胞系(9.1.1和BMM8),用IFN-γ和/或GM-CSF激活并感染克氏锥虫。我们的结果表明,克氏锥虫上调MPM以及两种巨噬细胞系(无论是否被IFN-γ激活)中GM-CSF的释放。GM-CSF的高自分泌产生或外源性GM-CSF的供应与TNF-α和NO的释放增加相关,从而使IFN-γ激活的MPM对克氏锥虫感染的控制得到改善。

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Relationship between granulocyte macrophage-colony stimulating factor, tumour necrosis factor-alpha and Trypanosoma cruzi infection of murine macrophages.粒细胞巨噬细胞集落刺激因子、肿瘤坏死因子-α与小鼠巨噬细胞克氏锥虫感染之间的关系。
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