Targeting ETosis by miR-155 inhibition mitigates mixed granulocytic asthmatic lung inflammation.

ABSTRACT: Asthma is phenotypically heterogeneous with several distinctive pathological mechanistic pathways. Previous studies indicate that neutrophilic asthma has a poor response to standard asthma treatments comprising inhaled corticosteroids. Therefore, it is important to identify critical factors that contribute to increased numbers of neutrophils in asthma patients whose symptoms are poorly controlled by conventional therapy. Leukocytes release chromatin fibers, referred to as extracellular traps (ETs) consisting of double-stranded (ds) DNA, histones, and granule contents. Excessive components of ETs contribute to the pathophysiology of asthma; however, it is unclear how ETs drive asthma phenotypes and whether they could be a potential therapeutic target. We employed a mouse model of severe ast

SUBMITTER: Kim JY 

PROVIDER: S-EPMC9360579 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature