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内源性白细胞介素-10在IgG免疫复合物诱导的肺损伤中的调节作用。

Regulatory effects of intrinsic IL-10 in IgG immune complex-induced lung injury.

作者信息

Shanley T P, Schmal H, Friedl H P, Jones M L, Ward P A

机构信息

Department of Pathology, University of Michigan Medical School, Ann Arbor 48109.

出版信息

J Immunol. 1995 Apr 1;154(7):3454-60.

PMID:7897226
Abstract

IL-10 has regulatory effects in vitro on cytokine production by activated macrophages. In the IgG immune complex model of lung injury, exogenously administered IL-10 has been shown to suppress in vivo formation of TNF-alpha, up-regulation of vascular ICAM-1, neutrophil recruitment, and ensuing lung injury. In the current study, we sought to determine whether endogenous IL-10 is playing a regulatory role in the lung inflammatory response. On the basis of lung mRNA and ELISA measurements, IL-10 induction was found during development of inflammation in the IgG immune complex model of lung injury. Blocking of IL-10 by Ab resulted in a 52% increase in lung vascular permeability, a 56% increase in TNF-alpha activity in bronchoalveolar lavage fluids, and a 47 to 48% increase in bronchoalveolar lavage neutrophils and lung myeloperoxidase content. These findings suggest that IL-10 is an important natural regulator of lung inflammatory injury after deposition of IgG immune complexes.

摘要

白细胞介素-10(IL-10)在体外对活化巨噬细胞产生细胞因子具有调节作用。在肺部损伤的IgG免疫复合物模型中,外源性给予的IL-10已被证明可在体内抑制肿瘤坏死因子-α(TNF-α)的形成、血管细胞间黏附分子-1(ICAM-1)的上调、中性粒细胞募集以及随之而来的肺损伤。在本研究中,我们试图确定内源性IL-10是否在肺部炎症反应中发挥调节作用。基于肺组织mRNA和酶联免疫吸附测定(ELISA)测量结果,在肺部损伤的IgG免疫复合物模型炎症发展过程中发现了IL-10的诱导。用抗体阻断IL-10导致肺血管通透性增加52%,支气管肺泡灌洗液中TNF-α活性增加56%,支气管肺泡灌洗中性粒细胞和肺髓过氧化物酶含量增加47%至48%。这些发现表明,IL-10是IgG免疫复合物沉积后肺部炎症损伤的重要天然调节因子。

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