白细胞介素-34在脂多糖诱导的急性肺损伤小鼠模型中诱导肺部炎症

T. Ebato, S. Ohta, Munehiro Yamaguchi, H. Mikuni, H. Ikeda, M. Jinno, K. Hirai, Y. Miyata, H. Inoue, T. Homma, Mayumi Yamamoto, S. Suzuki, A. Tanaka, H. Sagara
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引用次数: 0

摘要

细胞因子白介素-34 (IL-34)最近被描述。然而,它在肺部的作用尚不清楚。IL-34结合集落刺激因子-1受体,从而促进组织巨噬细胞的成熟和分化。巨噬细胞对气道炎症过程和急性肺损伤(ALI)至关重要。本研究旨在评价IL-34在ALI建立中的作用。收集支气管肺泡灌洗液(BALF)及肺组织。LPS对人外周血单核细胞THP-1和人气道上皮细胞BEAS-2B进行体外培养。THP-1细胞中TNF- α总含量高于TNF- α。此外,TNF- α刺激可诱导BEAS-2B细胞产生IL-34。这些结果提示,在lps诱导的急性肺损伤小鼠模型中,上皮细胞IL-34的诱导可增强肺部炎症和纤维化。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Interleukin-34 induces pulmonary inflammation in a murine model of lipopolysaccharide-induced acute lung injury
The cytokine interleukin-34 ( IL-34 ) was recently described. However, its role in the lungs is not well understood. IL-34 binds to the colony stimulating factor-1 receptor, thereby enhancing tissue macrophage maturation and differentiation. Macrophages are essential to the airway inflammation process and acute lung injury ( ALI ) . This study aimed to evaluate the role of IL-34 in ALI establishment. The bronchoalveolar lavage fluid ( BALF ) and lung tissues were collected. The cells of the human peripheral blood monocyte cell line THP-1 and the human airway epithelial cell line BEAS-2B were with LPS in vitro . The total in the than in the factor- α ( TNF- α) in THP-1 cells. Furthermore, TNF- α stimulation induced the IL-34 production in BEAS-2B cells. These results suggest that IL-34 induction in the epithelial cells may enhance pulmonary inflammation and fibrosis in the murine model of LPS-induced acute lung injury.
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