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首页> 外文期刊>Clinical and experimental allergy : >Airway epithelium-derived transforming growth factor-beta is a regulator of fibroblast proliferation in both fibrotic and normal subjects.
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Airway epithelium-derived transforming growth factor-beta is a regulator of fibroblast proliferation in both fibrotic and normal subjects.

机译：气道上皮来源的转化生长因子β是纤维化和正常受试者中成纤维细胞增殖的调节剂。

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BACKGROUND: In the healthy lung, airway epithelial cells (AEC) regulate fibroblast proliferation through release of soluble factors, such as prostaglandins and proteins. Fibroproliferative diseases and airway remodelling may result from an inadequate generation of suppressive factors by AEC or the inability of fibroblasts to respond to them appropriately. OBJECTIVE: The aim of this study was to study the effect of primary human AEC on the proliferation of fibroblasts obtained from healthy and fibrotic lungs in an interactive cell culture model. RESULTS: Conditioned medium (CM) from 14 out of 16 AEC lines significantly inhibited proliferation of normal human lung fibroblasts by 51.2+/-6.0%. The proliferation of fibroblasts derived from patients with lung fibrosis was equally inhibited by CM of AEC. The inhibitory effect of AEC-CM was completely reversed when fibroblasts were pre-incubated with 2.5 microm indomethacin. Furthermore, primary human AEC, but not fibroblasts, secrete TGF-beta, and the inhibitory effect of the AEC-CM was blocked by neutralizing anti-TGF-beta antibodies. CONCLUSION: These results demonstrate that AEC actively inhibit the proliferation of both normal and fibrotic fibroblasts via TGF-beta, which induces the prostaglandin E(2) synthesis in fibroblasts. The data indicate that proliferative lung diseases may be treated using the epithelial cell as the target of medication.
机译：背景：在健康的肺部，气道上皮细胞（AEC）通过释放前列腺素和蛋白质等可溶性因子来调节成纤维细胞的增殖。纤维增生性疾病和气道重塑可能是由于AEC产生的抑制因子不足或成纤维细胞无法对其做出适当反应而导致的。目的：本研究的目的是在交互式细胞培养模型中研究原代人AEC对健康肺和纤维化肺中成纤维细胞增殖的影响。结果：来自16个AEC系中的14个的条件培养基（CM）显着抑制了正常人肺成纤维细胞的增殖，其抑制率为51.2 +/- 6.0％。 AEC CM同样抑制肺纤维化患者来源的成纤维细胞增殖。当成纤维细胞与2.5微米消炎痛一起预孵育时，AEC-CM的抑制作用完全逆转。此外，原发性人类AEC而非成纤维细胞分泌TGF-β，并且中和抗TGF-β抗体可阻断AEC-CM的抑制作用。结论：这些结果表明，AEC通过TGF-beta积极抑制正常和纤维化成纤维细胞的增殖，从而诱导成纤维细胞中前列腺素E（2）的合成。数据表明，可以使用上皮细胞作为药物治疗靶点来治疗增生性肺部疾病。

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