Fluticasone propionate and increased risk of pneumonia in COPD: is it PAFR-dependent?
Sukhwinder Singh Sohal
Discipline of Laboratory Medicine, School of Health Sciences, Faculty of Health, University of Tasmania, Launceston, Australia
It was with great interest that I read the recent comprehensive review by Christer Janson et al1 published in the International Journal of COPD, where authors discussed the possible mechanisms behind the increased risk of pneumonia in COPD patients using inhaled corticosteroids (ICSs), especially with fluticasone propionate (FP), where the risk was highest.1 It is an important area, and it is encouraging and reassuring that leading clinical journals are recognizing this. Understanding the fundamental mechanisms behind pneumococcal infections is critical.2 I would like to suggest that a broader discussion of new insights into the potential mechanisms contributing to the increased adherence of pneumococcus to airway wall and particularly in response to FP might has been appropriate with this opportunity.
Christer Janson,1 Georgios Stratelis,1,2 Anna Miller-Larsson,3 Tim W Harrison,4 Kjell Larsson5
1Respiratory, Allergy and Sleep Research Unit, Department of Medical Sciences, Uppsala University, Uppsala, 2Respiratory, Inflammation and Autoimmunity, AstraZeneca Nordic, Södertälje, 3Respiratory GMed, AstraZeneca Gothenburg, Mölndal, Sweden; 4Nottingham Respiratory Research Unit, City Hospital Campus, University of Nottingham, Nottingham, UK; 5Lung and Airway Research, National Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
We thank Dr Sohal for his interest in our recently published manuscript discussing the scientific rationale for the possible inhaled corticosteroid (ICS) intraclass difference in the risk of pneumonia in COPD. His own work on platelet-activating factor receptor (PAFR) expression on airway epithelial cells in COPD patients shows a trend toward increased expression of PAFR by 6-month treatment with fluticasone propionate (FP), suggesting an increased rate of pneumococcal adhesion with FP, and hence the possible development of infection or pneumonia.1 This supports in part the work by Heijink et al2 that we cited in our paper.2
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