Antimacrophage chemokine treatment prevents neutrophil and macrophage influx in hyperoxia-exposed newborn rat lung.
Antimacrophage chemokine treatment prevents neutrophil and macrophage influx in hyperoxia-exposed newborn rat lung.
复制标题
抗巨噬细胞趋化因子治疗可防止中性粒细胞和巨噬细胞流入高氧暴露的新生大鼠肺部。
DOI：
10.1152/ajplung.00414.2002
复制
发表时间：
2004
期刊：
影响因子：
--
通讯作者：
AutenJr,RichardL
中科院分区：
文献类型：
--
作者：
Vozzelli,MichaelA;Mason,SNicholas;Whorton,MaryH;AutenJr,RichardL
巨噬细胞衍生的细胞因子可能在肺损伤中引发炎症反应。由于巨噬细胞内流是伴随着支气管肺发育不良发展的细胞炎症反应的一个显著特征，我们假设阻断巨噬细胞内流将减少整体细胞内流和氧化损伤。新生大鼠出生时暴露于95%O2或空气中1wk，高氧暴露后第3~5天给予抗单核细胞趋化蛋白-1(MCP-1)或免疫球蛋白G对照。与空气暴露对照相比，95%O2暴露和注射免疫球蛋白的新生大鼠肺泡灌洗液和组织切片中MCP-1水平升高。在1wk时，与免疫球蛋白对照组相比，抗单核细胞趋化蛋白-1抗体处理的幼鼠在支气管肺泡灌洗液中的白细胞数量减少，包括巨噬细胞和中性粒细胞。细胞因子诱导的中性粒细胞趋化因子-1是大鼠IL-8的类似物，在灌洗液中没有明显减少，但在抗MCP-1处理的小鼠肺细胞中减少。在抗MCP-1处理的幼鼠中，组织羰基，一种蛋白质氧化的指标，减少了。抗MCP-1治疗可防止高氧暴露新生大鼠中性粒细胞内流和减少蛋白质氧化。
Macrophage-derived cytokines may provoke the inflammatory response in lung injury. Because macrophage influx is a prominent feature of the cellular inflammatory response accompanying the development of bronchopulmonary dysplasia, we hypothesized that blocking macrophage influx would reduce overall cellular influx and oxidative damage. Newborn rats were exposed at birth to 95% O2or air for 1 wk, and hyperoxia-exposed pups were injected with anti-monocyte chemoattractant protein-1 (MCP-1) or IgG control ondays 3–5. MCP-1 was increased in bronchoalveolar lavage fluid and in histological sections from the 95% O2-exposed, IgG-injected pups compared with air-exposed controls. At 1 wk, anti-MCP-1-treated pups had reduced leukocyte numbers, both macrophages and neutrophils, in bronchoalveolar lavage fluid compared with IgG-treated controls. Cytokine-induced neutrophil chemoattractant-1, the rat analog of IL-8, was not significantly decreased in lavage fluid but was reduced in lung cells in anti-MCP-1-treated pups. Tissue carbonyls, a measure of protein oxidation, were decreased in anti-MCP-1-treated pups. Anti-MCP-1 treatment prevented neutrophil influx and reduced protein oxidation in hyperoxia-exposed newborn rats.