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首页> 外文期刊>American Journal of Physiology >Role of resident alveolar macrophages in leukocyte traffic into the alveolar air space of intact mice.
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Role of resident alveolar macrophages in leukocyte traffic into the alveolar air space of intact mice.

机译：常驻肺泡巨噬细胞在白细胞进入完整小鼠肺泡气隙中的作用。

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摘要

Intratracheal instillation of the monocyte chemoattractant JE/monocyte chemoattractant protein (MCP)-1 in mice was recently shown to cause increased alveolar monocyte accumulation in the absence of lung inflammation, whereas combined JE/MCP-1/lipopolysaccharide (LPS) challenge provoked acute lung inflammation with early alveolar neutrophil and delayed alveolar monocyte influx. We evaluated the role of resident alveolar macrophages (rAM) in these leukocyte recruitment events and related phenomena of lung inflammation. Depletion of rAM by pretreatment of mice with liposomal clodronate did not affect the JE/MCP-1-driven alveolar monocyte accumulation, despite the observation that rAM constitutively expressed the JE/MCP-1 receptor CCR2, as analyzed by flow cytometry and immunohistochemistry. In contrast, depletion of rAM largely suppressed alveolar cytokine release as well as neutrophil and monocyte recruitment profiles upon combined JE/MCP-1/LPS treatment. Despite this strongly attenuated alveolar inflammatory response, increased lung permeability was still observed in rAM-depleted mice undergoing JE/MCP-1/LPS challenge. Lung leakage was abrogated by codepletion of circulating neutrophils or administration of anti-CD18. Collectively, rAM are not involved in JE/MCP-1-driven alveolar monocyte recruitment in noninflamed lungs but largely contribute to the alveolar cytokine response and enhanced early neutrophil and delayed monocyte influx under inflammatory conditions (JE/MCP-1/LPS deposition). Loss of lung barrier function observed under these conditions is rAM independent but involves circulating neutrophils via beta(2)-integrin engagement.
机译：气管内滴注单核细胞趋化性JE /单核细胞趋化蛋白（MCP）-1在小鼠中可导致无肺炎症的情况下引起肺泡单核细胞积聚增加，而JE / MCP-1 /脂多糖（LPS）联合刺激可引起急性肺早期肺泡中性粒细胞发炎和肺泡单核细胞延迟流入。我们评估了居民肺泡巨噬细胞（rAM）在这些白细胞募集事件和相关的肺部炎症现象中的作用。尽管通过流式细胞仪和免疫组织化学分析发现rAM组成型表达了JE / MCP-1受体CCR2，但通过脂质体氯膦酸盐预处理小鼠耗竭的rAM并没有影响JE / MCP-1驱动的肺泡单核细胞的积累。相反，在联合JE / MCP-1 / LPS治疗后，rAM的耗竭在很大程度上抑制了肺泡细胞因子的释放以及中性粒细胞和单核细胞的募集。尽管这种强烈减弱的肺泡炎症反应，仍然在经历JE / MCP-1 / LPS攻击的rAM耗竭小鼠中观察到肺通透性增加。循环中性粒细胞的代码缺失或抗CD18的施用消除了肺的渗漏。总的来说，rAM不参与非发炎肺部JE / MCP-1驱动的肺泡单核细胞募集，但在炎性条件下（JE / MCP-1 / LPS沉积）在很大程度上促进了肺泡细胞因子的反应并增强了早期中性粒细胞和单核细胞的延迟流入。在这些情况下观察到的肺屏障功能丧失与rAM无关，但涉及通过β（2）-整合素参与的循环中性粒细胞。

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