Resolving Viral-Induced Secondary Bacterial Infection in COPD: A Concise Review

Wang, H, Anthony, D, Selemidis, S, Vlahos, R and Bozinovski, S 2018, 'Resolving Viral-Induced Secondary Bacterial Infection in COPD: A Concise Review', Frontiers in Immunology, vol. 9, pp. 1-7.


Document type: Journal Article
Collection: Journal Articles

Title Resolving Viral-Induced Secondary Bacterial Infection in COPD: A Concise Review
Author(s) Wang, H
Anthony, D
Selemidis, S
Vlahos, R
Bozinovski, S
Year 2018
Journal name Frontiers in Immunology
Volume number 9
Start page 1
End page 7
Total pages 7
Publisher Frontiers Research Foundation
Abstract Chronic obstructive pulmonary disease (COPD) is a leading cause of disability and death world-wide, where chronic inflammation accelerates lung function decline. Pathological inflammation is worsened by chronic bacterial lung infections and susceptibility to recurrent acute exacerbations of COPD (AECOPD), typically caused by viral and/or bacterial respiratory pathogens. Despite ongoing efforts to reduce AECOPD rates with inhaled corticosteroids, COPD patients remain at heightened risk of developing serious lung infections/AECOPD, frequently leading to hospitalization and infection-dependent delirium. Here, we review emerging mechanisms into why COPD patients are susceptible to chronic bacterial infections and highlight dysregulated inflammation and production of reactive oxygen species (ROS) as central causes. This underlying chronic infection leaves COPD patients particularly vulnerable to acute viral infections, which further destabilize host immunity to bacteria. The pathogeneses of bacterial and viral exacerbations are significant as clinical symptoms are more severe and there is a marked increase in neutrophilic inflammation and tissue damage. AECOPD triggered by a bacterial and viral co-infection increases circulating levels of the systemic inflammatory marker, serum amyloid A (SAA). SAA is a functional agonist for formyl peptide receptor 2 (FPR2/ALX), where it promotes chemotaxis and survival of neutrophils. Excessive levels of SAA can antagonize the protective actions of FPR2/ALX that involve engagement of specialized pro-resolving mediators, such as resolvin-D1. We propose that the anti-microbial and anti-inflammatory actions of specialized pro-resolving mediators, such as resolvin-D1 should be harnessed for the treatment of AECOPD that are complicated by the co-pathogenesis of viruses and bacteria.
Subject Respiratory Diseases
Keyword(s) COPD-chronic obstructive pulmonary disease
exacerbation
influenza (flu)
secondary infection
co-infection
resolvin D1 (RvD1)
serum amyloid A (SAA)
pneumococcus (Streptococcus pneumoniae)
DOI - identifier 10.3389/fimmu.2018.02345
Copyright notice Copyright © 2018 Wang, Anthony, Selemidis, Vlahos and Bozinovski. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY).
ISSN 1664-3224
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