支气管收缩
支气管痉挛
炎症
粘液
气道
机械转化
哮喘
医学
分泌物
免疫学
细胞生物学
内科学
生物
麻醉
生态学
作者
Dustin C. Bagley,Tobias Russell,Elena Ortiz-Zapater,K. J. Fox,Paulina Frances Redd,Merry Joseph,Caitlin Rice,Christopher A. Reilly,Maddy Parsons,Jody Rosenblatt
标识
DOI:10.1101/2023.08.04.551943
摘要
ABSTRACT Asthma is deemed an inflammatory disease, yet the defining diagnostic symptom is mechanical bronchoconstriction. We previously discovered a conserved process that drives homeostatic epithelial cell death in response to mechanical cell crowding called cell extrusion( 1, 2 ). Here, we show that the pathological crowding of a bronchoconstrictive attack causes so much epithelial cell extrusion that it damages the airways, resulting in inflammation and mucus secretion. While relaxing airways with the rescue treatment albuterol did not impact these responses, inhibiting live cell extrusion signaling during bronchoconstriction prevented all these symptoms. Our findings propose a new etiology for asthma, dependent on the mechanical crowding of a bronchoconstrictive attack. Our studies suggest that blocking epithelial extrusion, instead of ensuing downstream inflammation, could prevent the feed-forward asthma inflammatory cycle.
科研通智能强力驱动
Strongly Powered by AbleSci AI