3 years ago

Protease-Activated Receptor-2 blockade inhibits changes seen in a chronic murine asthma model

Harissios Vliagoftis, Yahya Fiteih, Muhammad Asaduzzaman, Courtney Davidson, Lakshmi Puttagunta, Drew Nahirney
Proteinase-Activated Receptor-2 (PAR2) is a G protein-coupled receptor activated by serine proteinases. We have shown that PAR2 activation in the airways is involved in the development of allergic inflammation and airway hyperresponsiveness (AHR) in acute murine models. We hypothesize that functional inhibition of PAR2 prevents allergic inflammation, AHR and airway remodeling in chronic allergic airway inflammation models. We developed a 12 week model of cockroach extract (CE)-mediated AHR, airway inflammation and remodeling in BALB/c. These mice exhibit AHR, increased numbers of eosinophils in bronchoalveolar lavage (BAL) and increased collagen content in the lung tissue compared to saline controls. Administration of an anti-PAR2 antibody, SAM-11, after the initial development of airway inflammation significantly inhibited all these parameters. Our data demonstrate that PAR2 signaling plays a key role in CE-induced AHR and airway inflammation/remodeling and that targeting PAR2 activation may be a successful therapeutic strategy for allergic asthma. This article is protected by copyright. All rights reserved.

Publisher URL: http://onlinelibrary.wiley.com/resolve/doi

DOI: 10.1111/all.13313

You might also like
Never Miss Important Research

Researcher is an app designed by academics, for academics. Create a personalised feed in two minutes.
Choose from over 15,000 academics journals covering ten research areas then let Researcher deliver you papers tailored to your interests each day.

  • Download from Google Play
  • Download from App Store
  • Download from AppInChina

Researcher displays publicly available abstracts and doesn’t host any full article content. If the content is open access, we will direct clicks from the abstracts to the publisher website and display the PDF copy on our platform. Clicks to view the full text will be directed to the publisher website, where only users with subscriptions or access through their institution are able to view the full article.