It Takes 1 for Type 2: IL-1 Receptor Mediates Eosinophilia in Scnn1b Transgenic Mice.
It Takes 1 for Type 2: IL-1 Receptor Mediates Eosinophilia in Scnn1b Transgenic Mice.
复制标题
2 型需要 1：IL-1 受体介导 Scnn1b 转基因小鼠中的嗜酸性粒细胞增多。
DOI：
10.1165/rcmb.2019-0332ed
复制
发表时间：
2020
影响因子：
6.4
通讯作者：
Evans,ChristopherM
中科院分区：
文献类型：
--
作者：
Jaramillo,AnaM;Evans,ChristopherM
A major phenotype that is present in muco-obstructive lung diseases such as asthma and chronic obstructive pulmonary disease is eosinophilic inflammation. Eosinophils contribute to airway hyperresponsiveness, and eosinophil-generated oxidants may further promote mucus plug formation (1). Scnn1b-Tg mice overexpress a subunit of the epithelial sodium channel that results in ion transport imbalance, leading to airway surface dehydration, increased mucin concentration, and reduced mucociliary clearance. Together, these factors cause severe mucus obstruction.In addition, Scnn1b-Tg mice exhibit prominent type 2 inflammation during the first weeks of life. Previous studies have linked IL-1 receptor (IL-1R) signaling to the recruitment of leukocytes in allergic models (2, 3). However, how IL-1R participates in spontaneous airway eosinophilia is still unknown. In this issue of the Journal, Brown and colleagues (pp. 300-309) provide insight into the role of IL-1R signaling in spontaneous airway eosinophilia and type 2 inflammation in juvenile Scnn1b-Tg mice (4).
