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Bronchial platelet-activating factor receptor in chronic obstructive pulmonary disease
Reetika Suri1, Patrick Mallia2, Joanne E Martin1
1Blizard Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London E1 2AT, UK.
Respiratory Medicine
|April 2, 2014
Summary
Bronchial platelet-activating factor receptor (PAFR) mRNA is elevated in smokers and those with COPD. Rhinovirus infection did not further increase PAFR mRNA in these groups, suggesting PAFR is not a target for rhinovirus-induced exacerbations.
Area of Science:
- Pulmonary Medicine
- Microbiology
- Immunology
Background:
- Bacteria use phosphorylcholine (ChoP) to bind airway cells via the platelet-activating factor receptor (PAFR).
- Cigarette smoke and rhinovirus (RV) infection increase PAFR-dependent bacterial adhesion in vitro.
- The impact of chronic obstructive pulmonary disease (COPD) on smoke-induced PAFR upregulation is unknown.
Purpose of the Study:
- To investigate if bronchial PAFR mRNA expression is increased in smokers with COPD.
- To determine if RV infection further elevates PAFR mRNA in smokers and COPD patients.
Main Methods:
- Endobronchial biopsies were collected from non-smokers, smokers, and COPD patients before and after RV16 infection.
- PAFR mRNA expression was quantified using RT-qPCR.
- PAFR distribution was analyzed via immunohistochemistry.
Main Results:
- Baseline PAFR mRNA levels were significantly higher in smokers and COPD patients compared to non-smokers.
- RV16 infection did not lead to increased PAFR mRNA expression in any group.
- PAFR was primarily localized to the bronchial epithelium and submucosal glands.
Conclusions:
- Elevated endobronchial PAFR mRNA is present in both smokers and individuals with COPD.
- RV16 infection does not appear to upregulate bronchial PAFR mRNA in smokers or COPD patients.
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