Royce Simon G, Lim Clarice, Muljadi Ruth C, Tang Mimi L K
Allergy and Immune Disorders, Murdoch Children's Research Institute, Royal Children's Hospital, Parkville, Australia.
J Asthma. 2011 Sep;48(7):653-9. doi: 10.3109/02770903.2011.599906. Epub 2011 Jul 28.
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.
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.
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.
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.
上皮剥脱和化生在气道重塑和哮喘的发病机制中具有重要作用。三叶因子2(TFF2)是一类参与胃肠道上皮保护和修复的肽家族成员,也在气道黏膜中分泌。
我们通过组织学和形态计量学分析,研究了TFF2在哮喘的两种相关动物模型中对气道重塑的作用,这两种模型分别是变应性气道疾病的卵清蛋白模型和烟曲霉抗原致敏模型,所用肺组织来自TFF2基因缺陷小鼠。
在卵清蛋白模型中,与野生型(WT)小鼠相比,TFF2基因缺陷小鼠杯状细胞增生增加,但上皮未增厚。在烟曲霉模型中,TFF2基因缺陷小鼠杯状细胞增生也增加,并且与WT对照相比,烟曲霉致敏小鼠的上皮厚度也增加。TFF2缺乏还与上皮下胶原层厚度增加有关。
当前研究证明了TFF2在气道疾病小鼠模型气道重塑中的作用。有必要进一步研究TFF2的作用机制及其在哮喘中的作用。