| Literature DB >> 32503090 |
Oisín F McElvaney1, Mark P Murphy1, Emer P Reeves1, Noel G McElvaney1.
Abstract
For many years, the lung disease associated with alpha-1 antitrypsin (AAT) deficiency (AATD) was perceived as being secondary to an imbalance between this serine protease inhibitor and the target protease, neutrophil elastase (NE). More recently, a greater understanding of the pathways leading to lung inflammation has shed light on new potential attributes and presented AATD as an inflammatory condition in which proteases and neutrophils still play a major role, but in which pro-inflammatory cytokines, either induced by the actions of NE or by other pro-inflammatory processes normally modulated by AAT, are involved. In this review, we will look at the various cytokines centrally involved in AATD lung disease, and how a greater understanding of their contribution may help development of targeted therapies. JCOPDFEntities:
Keywords: alpha-1 antitrypsin; cytokines; inflammation; interleukin-8; neutrophils
Year: 2020 PMID: 32503090 PMCID: PMC7857705 DOI: 10.15326/jcopdf.7.3.2019.0171
Source DB: PubMed Journal: Chronic Obstr Pulm Dis ISSN: 2372-952X