Human alveolar epithelial cells induce nitric oxide synthase‐2 expression in alveolar macrophages
Human alveolar epithelial cells induce nitric oxide synthase‐2 expression in alveolar macrophages
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人肺泡上皮细胞诱导肺泡巨噬细胞表达一氧化氮合酶-2
DOI：
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发表时间：
2002
影响因子：
24.3
通讯作者：
J. Müller
中科院分区：
文献类型：
--
作者：
D. Pechkovsky;G. Zissel;C. Stamme;T. Goldmann;H. Jaffe;M. Einhaus;C. Taube;H. Magnussen;M. Schlaak;J. Müller
假设人肺泡巨噬细胞（AM）和肺泡上皮细胞之间的细胞间相互作用可能是导致肺泡壁和/或AM组成细胞表达一氧化氮合酶-2（NOS 2）信使核糖核酸（mRNA）和蛋白质的重要因素。从肺恶性肿瘤患者的肺切除的正常部分分离的人AM和肺泡上皮细胞II型（AECII）的NOS 2 mRNA和蛋白表达模式进行了测定。此外，研究了在促炎细胞因子白细胞介素（IL）-1 β、肿瘤坏死因子（TNF）-α、干扰素（IFN）-γ或脂多糖（LPS）存在下，与自体AECII共培养的人AM中NOS 2 mRNA的表达。还研究了人表面活性蛋白A（SP-A）对人AM中IFN-γ介导的NOS2 mRNA表达的影响。在新鲜分离的、未刺激的或细胞激动剂刺激的AECII中均未检测到NOS2 mRNA和蛋白。与此相反，新鲜分离的AM支气管肺泡灌洗液或肺组织样本表达免疫反应NOS 2蛋白，但没有NOS 2 mRNA可以通过逆转录聚合酶链反应检测。所有的刺激都不能诱导人AM中NOS2 mRNA的表达。只有在IFN-γ存在下的AMAECII共培养导致NOS2 mRNA和蛋白表达。肺组织外植体上的NOS 2 mRNA的原位杂交和AMAECII共培养物的cytospin制备物的免疫组织化学染色表明，NOS 2在AM中表达，但不在AECII中。用SP-A替代AECII不能再现这种共培养效应。这些数据提供了控制下呼吸道中人一氧化氮合酶-2表达的调节网络的证据。
It was hypothesized that celltocell interaction between human alveolar macrophages (AM) and alveolar epithelium, might be an important factor leading to nitric oxide synthase‐2 (NOS2) messenger ribonucleic acid (mRNA) and protein expression by constituent cells of the alveolar wall and/or AM. NOS2 mRNA and the protein expression patterns of human AM and alveolar epithelial cells type II (AECII) isolated from normal parts of lung resections of patients with pulmonary malignancies were determined. In addition, NOS2 mRNA expression in human AM cocultured with autologous AECII in the presence of proinflammatory cytokines interleukin (IL)‐1β, tumour necrosis factor (TNF)‐α, interferon (IFN)‐γ or lipopolysaccharide (LPS) was investigated. The effect of human surfactant protein‐A (SP‐A) on IFN‐γ‐mediated NOS2 mRNA expression in human AM was also studied. Neither NOS2 mRNA nor protein could be detected in freshly isolated, unstimulated or cytokinestimulated AECII. In contrast, freshly isolated AM from bronchoalveolar lavage or lung tissue samples expressed immunoreactivity for NOS2 protein, but no NOS2 mRNA could be detected by reverse transcriptase polymerase chain reaction. All stimuli tested failed to induce NOS2 mRNA expression in human AM in vitro. Only AMAECII coculture in the presence of IFN‐γ led to NOS2 mRNA and protein expression. In situ hybridization of NOS2 mRNA on lung tissue explants and immunohistochemical staining of cytospin preparations of AMAECII cocultures demonstrated that NOS2 is expressed in AM but not in AECII. This coculture effect could not be reproduced by substitution of AECII with SP‐A. These data give evidence of a regulatory network controlling human nitric oxide synthase‐2 expression in the lower respiratory tract.
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DOI：
10.1089/jir.1992.12.307
发表时间：
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期刊：
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影响因子：
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作者：
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2000
期刊：
American journal of respiratory cell and molecular biology.
影响因子：
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DOI：
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发表时间：
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影响因子：
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DOI：
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期刊：
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影响因子：
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DOI：
10.1165/ajrcmb.12.6.7539274
发表时间：
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期刊：
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影响因子：
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