tetano
Editor, Senior Moderator
Front Immunol. 2018 Oct 16;9:2345. doi: 10.3389/fimmu.2018.02345. eCollection 2018.
[h=1]Resolving Viral-Induced Secondary Bacterial Infection in COPD: A Concise Review.[/h] Wang H[SUP]1[/SUP], Anthony D[SUP]1[/SUP], Selemidis S[SUP]1[/SUP], Vlahos R[SUP]1[/SUP], Bozinovski S[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] 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.
[h=4]KEYWORDS:[/h] COPD-chronic obstructive pulmonary disease; co-infection; exacerbation; influenza (flu); pneumococcus (Streptococcus pneumoniae); resolvin D1 (RvD1); secondary infection; serum amyloid A (SAA)
PMID: 30459754 PMCID: PMC6232692 DOI: 10.3389/fimmu.2018.02345
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[h=1]Resolving Viral-Induced Secondary Bacterial Infection in COPD: A Concise Review.[/h] Wang H[SUP]1[/SUP], Anthony D[SUP]1[/SUP], Selemidis S[SUP]1[/SUP], Vlahos R[SUP]1[/SUP], Bozinovski S[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] 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.
[h=4]KEYWORDS:[/h] COPD-chronic obstructive pulmonary disease; co-infection; exacerbation; influenza (flu); pneumococcus (Streptococcus pneumoniae); resolvin D1 (RvD1); secondary infection; serum amyloid A (SAA)
PMID: 30459754 PMCID: PMC6232692 DOI: 10.3389/fimmu.2018.02345
Free full text