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首页> 外文期刊>Clinical and experimental allergy : >Endothelin‐1 mediates Aspergillus fumigatus Aspergillus fumigatus ‐induced airway inflammation and remodelling
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Endothelin‐1 mediates Aspergillus fumigatus Aspergillus fumigatus ‐induced airway inflammation and remodelling

机译：内皮素-1介质曲霉曲霉曲霉（Aspergillus fumigatus曲霉）诱导的气道炎症和重塑

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Summary Background Asthma is a chronic inflammatory condition of the airways and patients sensitized to airborne fungi such as Aspergillus fumigatus have more severe asthma. Thickening of the bronchial subepithelial layer is a contributing factor to asthma severity for which no current treatment exists. Airway epithelium acts as an initial defence barrier to inhaled spores, orchestrating an inflammatory response and contributing to subepithelial fibrosis. Objective We aimed to analyse the production of pro‐fibrogenic factors by airway epithelium in response to A?fumigatus , in order to propose novel anti‐fibrotic strategies for fungal‐induced asthma. Methods We assessed the induction of key pro‐fibrogenic factors, TGF‐β1, TGF‐β2, periostin and endothelin‐1, by human airway epithelial cells and in mice exposed to A?fumigatus spores or secreted fungal factors. Results Aspergillus fumigatus specifically caused production of endothelin‐1 by epithelial cells in vitro but not any of the other pro‐fibrogenic factors assessed. A?fumigatus also induced endothelin‐1 in murine lungs, associated with extensive inflammation and airway remodelling. Using a selective endothelin‐1 receptor antagonist, we demonstrated for the first time that endothelin‐1 drives many features of airway remodelling and inflammation elicited by A?fumigatus . Conclusion Our findings are consistent with the hypothesis that elevated endothelin‐1 levels contribute to subepithelial thickening and highlight this factor as a possible therapeutic target for difficult‐to‐treat fungal‐induced asthma.
机译：发明内容背景哮喘是气道的慢性炎症状况，患者敏感到空气中的真菌，如曲霉菌灰患有更严重的哮喘。支气管上皮层的增厚是对哮喘严重程度的贡献因子，没有存在电流处理。气道上皮充当吸入孢子的初始防御障碍，促进炎症反应并导致耻骨纤维化。目的旨在通过气道上皮响应a？fumigatus来分析促纤维原纤维导管的生产，以提出用于真菌诱导的哮喘的新型抗纤维化策略。方法评估人类气道上皮细胞和暴露于a？Fumigatus孢子或分泌的真菌因子的小鼠的关键促纤维因子，TGF-β1，TGF-β2，PERIOSTIN和内皮蛋白-1的诱导。结果Aspergillus Fumigatus专门通过上皮细胞在体外产生内皮素-1的产生，但不是评估的任何其他促纤纤遗传因素。 a？fumigatus还诱导鼠肺的内皮素-1，与广泛的炎症和气道重塑相关。使用选择性内皮素-1受体拮抗剂，我们首次证明了内皮素-1驱动了呼吸道重塑的许多特征和由a uumigatus引起的炎症。结论我们的研究结果与内皮素-1水平升高的假设一致，促使耻骨增厚，并突出了该因素作为难以治疗的真菌诱导的哮喘的可能治疗靶标。

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