胸腺基质淋巴细胞生成素
呼吸上皮
上皮
免疫学
免疫系统
炎症
生物
细胞生物学
气道
间质细胞
医学
病理
外科
作者
Gilda Varricchi,Christopher Brightling,Christopher Grainge,Bart N. Lambrecht,Pascal Chanez
出处
期刊:The European respiratory journal
[European Respiratory Society]
日期:2024-04-01
卷期号:63 (4): 2301619-2301619
被引量:6
标识
DOI:10.1183/13993003.01619-2023
摘要
Asthma is a chronic, heterogeneous disease of the airways, often characterised by structural changes known collectively as airway remodelling. In response to environmental insults, including pathogens, allergens and pollutants, the epithelium can initiate remodelling via an inflammatory cascade involving a variety of mediators that have downstream effects on both structural and immune cells. These mediators include the epithelial cytokines thymic stromal lymphopoietin, interleukin (IL)-33 and IL-25, which facilitate airway remodelling through cross-talk between epithelial cells and fibroblasts, and between mast cells and airway smooth muscle cells, as well as through signalling with immune cells such as macrophages. The epithelium can also initiate airway remodelling independently of inflammation in response to the mechanical stress present during bronchoconstriction. Furthermore, genetic and epigenetic alterations to epithelial components are believed to influence remodelling. Here, we review recent advances in our understanding of the roles of the epithelium and epithelial cytokines in driving airway remodelling, facilitated by developments in genetic sequencing and imaging techniques. We also explore how new and existing therapeutics that target the epithelium and epithelial cytokines could modify airway remodelling.
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