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Prepublished online as a Blood First Edition Paper on September 22, 2003; DOI 10.1182/blood-2003-05-1707.
Submitted May 30, 2003
Accepted August 28, 2003
Platelets are necessary for airway wall remodelling in a murine model of chronic allergic inflammation
Simon C Pitchford, Yanira Riffo-Vasquez, Ana Sousa, Stefania Momi, Paolo Gresele, Domenico Spina*, and Clive P Page
Sackler Institute of Pulmonary Pharmacology, GKT School of Biomedical Sciences, Kings College London, London, United Kingdom
Department of Internal Medicine, Section of Internal and Cardiovascular Medicine, University of Perugia, Perugia, Italy
* Corresponding author; email: domenico.spina{at}kcl.ac.uk.
Asthma is associated with airways remodelling. Evidence of platelet recruitment to the lungs of asthmatics after allergen exposure suggests they participate in various aspects of asthma, although their importance is unknown in the context of airway remodelling, their involvement in atherosclerosis is established. Studies from our laboratory have shown a requirement for platelets in pulmonary leukocyte recruitment in a murine model of allergic lung inflammation. Presently, the effects of platelet depletion and corticosteroid administration on airway remodelling and lung function were examined. Ovalbumin (OVA)-sensitised mice, exposed to aerosolised OVA for eight weeks, demonstrated epithelial and smooth muscle thickening, and sub-epithelial reticular fibre deposition in the distal airways. The depletion of platelets via an immunological (anti-platelet anti-sera) or non-immunological (busulfan) method, markedly reduced airway remodelling. In contrast, dexamethasone administration did not affect epithelial thickening or sub-epithelial fibrosis, despite significantly inhibiting leukocyte recruitment. Thus, pathways leading to certain aspects of airway remodelling may not depend on leukocyte recruitment, whilst platelet activation is obligatory. OVA-sensitised mice exhibited airway hyperresponsiveness (AHR) compared to sham-sensitised mice following chronic OVA exposure. Neither platelet depletion nor dexamethasone administration inhibited AHR, thus mechanisms other than inflammation and airway remodelling maybe involved in the pathogenesis of AHR.
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