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Does upregulated host cell receptor expression provide a link between bacterial adhesion and chronic respiratory
Ronan F O'Toole1, Shakti D Shukla2, Eugene H Walters2
1School of Medicine, Faculty of Health, University of Tasmania, Medical Science 1, 17 Liverpool Street, Hobart, TAS, 7000, Australia. ronan.otoole@utas.edu.au.
Smokers and COPD patients show increased platelet-activating factor receptor (PAFr) in airways. Blocking PAFr reduces bacterial adhesion, suggesting it as a target for chronic respiratory infections.
Area of Science:
- Pulmonary Medicine
- Microbiology
- Immunology
Background:
- Platelet-activating factor receptor (PAFr) expression is elevated in the respiratory epithelium of smokers and patients with chronic obstructive pulmonary disease (COPD).
- Increased PAFr expression correlates with enhanced adhesion of non-typable *Haemophilus influenzae* and *Streptococcus pneumoniae*, key pathogens in COPD exacerbations.
Purpose of the Study:
- To investigate the role of upregulated epithelial receptors, specifically PAFr, in bacterial adhesion and chronic respiratory infections.
- To explore the potential of targeting temporally upregulated host receptors as a therapeutic strategy against bacterial infections.
Main Methods:
- Assessed PAFr expression in respiratory epithelium.
- Quantified bacterial adhesion to human bronchial epithelial cells.
- Evaluated the effect of a PAFr antagonist on bacterial adhesion.
Main Results:
- Elevated PAFr expression was observed in smokers and COPD patients.
- Higher PAFr levels correlated with increased adhesion of *H. influenzae* and *S. pneumoniae*.
- A PAFr antagonist significantly reduced bacterial adhesion to control levels.
Conclusions:
- Upregulated epithelial receptors like PAFr in response to cigarette smoke can be targeted to block chronic bacterial infections in the lower respiratory tract.
- Adhesion to temporally upregulated host receptors may represent a common mechanism in chronic bacterial diseases, offering a potential therapeutic target.
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