Emerging therapeutic targets and preclinical models for severe asthma. (1st September 2020)

• Record Type: Journal Article
• Authors: Galvão, Izabela; Kim, Richard Y.; Shen, Sijie; Budden, Kurtis F.; Vieira, Angélica T.; Hansbro, Philip M.
• Is Part Of: Expert opinion on therapeutic targets. Volume 24:Number 9(2020:Sep.)
• Page Start: 845
• Page End: 857
• Publication Date: 2020-09-01
• Subjects: Inflammation -- severe asthma -- preclinical models -- novel therapies; Drugs -- Research -- Periodicals; 615.072
• DOI: 10.1080/14728222.2020.1786535
• Languages: English
• ISSNs: 1744-7631

Abstract

ABSTRACT: Introduction: Asthma is a heterogeneous disease with complex multifactorial causes. It is possible to subclassify asthma into different phenotypes that have distinct immunological features. Eosinophilic asthma is a well-known phenotype of severe asthma; however, a large body of clinical and experimental evidence strongly associates persistent airway inflammation, including the accumulation of neutrophils in the bronchial mucosa, and resistance to corticosteroid therapy and non-Type-2 immune responses with severe asthma. Importantly, mainstay therapies are often ineffective in severe asthma and effective alternatives are urgently needed. Areas covered: Here, we discussed recently developed mouse models of severe asthma that recapitulates key features of the disease in humans. We also provide findings from clinically relevant experimental models that have identified potential therapeutic targets for severe asthma. The most relevant publications on the topic of interest were selected from PubMed. Expert commentary: Increasing the understanding of disease-causing mechanisms in severe asthma may lead to the identification of novel therapeutic targets and the development of more effective therapies. Intense research interest into investigating the pathophysiological mechanisms of severe asthma has driven the development and interrogation of a myriad of mouse models that aim to replicate hallmark features of severe asthma in humans.