Human alveolar macrophage inhibition of lung fibroblast growth. A prostaglandin-dependent process.
Human alveolar macrophage inhibition of lung fibroblast growth. A prostaglandin-dependent process.
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DOI：
10.1164/arrd.1985.131.1.94
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发表时间：
2015-05
期刊：
影响因子：
--
通讯作者：
J. Elias;M. Rossman;R. Zurier;R. Daniele
中科院分区：
文献类型：
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作者：
J. Elias;M. Rossman;R. Zurier;R. Daniele
控制人肺纤维化的过程知之甚少。单核细胞可能是成纤维细胞功能的重要调节者，而肺泡巨噬细胞（AM）是人肺的主要单核吞噬细胞。为了进一步了解肺中AM-成纤维细胞相互作用，获得来自未刺激和刺激的粘附人AM的上清液，并表征其对人肺成纤维细胞的对数期生长的影响。肺泡巨噬细胞上清液以剂量依赖性方式抑制成纤维细胞生长。这种抑制是热稳定（56 ℃，1小时）、不可透析（分子量截止值，12，000道尔顿）、可溶性因子的结果，其优先由较小和较密集的巨噬细胞亚群产生。AM上清液的抑制能力与其刺激成纤维细胞前列腺素产生的能力直接相关。阻断成纤维细胞前列腺素的产生可以逆转AM上清液对成纤维细胞生长的抑制。因此，AM对成纤维细胞生长的抑制可能部分由成纤维细胞前列腺素的产生介导。肺泡巨噬细胞对成纤维细胞生长的抑制在预防正常人的纤维化和/或抑制肺部炎症所见的纤维化反应中可能是重要的。
The processes controlling fibrosis in the human lung are poorly understood. Mononuclear cells may be important regulators of fibroblast function, and the alveolar macrophage (AM) is the major mononuclear phagocyte of the human lung. To further understand AM-fibroblast interactions in the lung, supernatants from unstimulated and stimulated adherent human AM were obtained and their effect on the log phase growth of human lung fibroblasts was characterized. Alveolar macrophage supernatants inhibited fibroblast growth in a dose-dependent fashion. This inhibition was the result of a heat-stable (56 degrees C, 1 h), nondialyzable (molecular weight cutoff, 12,000 daltons), soluble factor(s), which was preferentially elaborated by smaller and denser macrophage subpopulations. The inhibitory capacity of an AM supernatant was directly related to its capacity to stimulate fibroblast prostaglandin production. Blocking fibroblast prostaglandin production reversed the inhibition of fibroblast growth caused by AM supernatants. Thus, AM inhibition of fibroblast growth may be mediated in part by fibroblast prostaglandin production. Alveolar macrophage inhibition of fibroblast growth may be important in preventing fibrosis in normal persons and/or in inhibiting the fibrotic response seen with pulmonary inflammation.