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Trefoil factor 2 regulates airway remodeling in animal models of asthma.

机译:三叶因子2调节哮喘动物模型中的气道重塑。

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摘要

BACKGROUND: Epithelial denudation and metaplasia are important in the pathogenesis of airway remodeling and asthma. Trefoil factor 2 (TFF2) is a member of a family of peptides involved in protection and healing of the gastrointestinal epithelium but which are also secreted in the airway mucosa. METHODS: We investigated the role of TFF2 in airway remodeling by histological and morphometric analysis of lung tissue from TFF2-deficient mice subjected to two relevant animal models of asthma: an ovalbumin model of allergic airways disease and an Aspergillus fumigatus antigen sensitization model. RESULTS: In the ovalbumin model TFF2-deficient mice had increased goblet cell hyperplasia, but not epithelial thickening compared to wild-type (WT) counterparts. In the Aspergillus model TFF2-deficient mice also had increased goblet cell hyperplasia, and epithelial thickness was also increased in the Aspergillus-sensitized mice compared to WT controls. TFF2 deficiency was also associated with increased subepithelial collagen layer thickness. DISCUSSION: The current study demonstrates a role of TFF2 in airway remodeling in mouse models of airway disease. Further studies into the mechanisms of action of TFF2 and its role in asthma are warranted.
机译:背景:上皮剥脱和化生在气道重塑和哮喘的发病机制中很重要。三叶因子2(TFF2)是与胃肠道上皮的保护和愈合有关的一系列肽的成员,但它们也分泌在气道粘膜中。方法:我们通过对患有两种相关哮喘模型的TFF2缺陷小鼠的肺组织进行组织学和形态计量学分析,研究了TFF2在气道重塑中的作用:过敏性气道疾病的卵清蛋白模型和烟曲霉抗原致敏模型。结果:在卵清蛋白模型中,与野生型(WT)相比,TFF2缺陷型小鼠的杯状细胞增生增加,但上皮增厚没有。在曲霉菌模型中,与野生型对照相比,TFF2缺陷型小鼠的杯状细胞增生也增加,并且在曲霉菌敏感的小鼠中上皮厚度也增加。 TFF2缺乏症也与上皮下胶原层厚度增加有关。讨论:本研究证明了TFF2在气道疾病小鼠模型中的气道重塑中的作用。有必要进一步研究TFF2的作用机理及其在哮喘中的作用。

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