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Published ahead of print on December 20, 2007, doi:10.1164/rccm.200702-214OC

Am. J. Respir. Crit. Care Med., Volume 177, Number 6, March 2008, 604-612

A more recent version of this article appeared on March 15, 2008
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Submitted on February 8, 2007
Accepted on December 20, 2007

Allergen Induces the Migration of Platelets to Lung Tissue in Allergic Asthma

Simon C Pitchford1, Stefania Momi2, Stefano Baglioni3, Lucio Casali2, Silvia Giannini2, Roberta Rossi2, Clive P Page4, and Paolo Gresele2*

1 Department of Internal Medicine, Division of Internal and Cardiovascular Medicine, University of Perugia, Perugia, Italy; Sackler Institute of Pulmonary Pharmacology, Pharmaceutical Sciences Research Division, King's College London, London, United Kingdom; Leukocyte Biology Section, National Heart and Lung Institute, Imperial College London, London, United Kingdom, 2 Department of Internal Medicine, Division of Internal and Cardiovascular Medicine, University of Perugia, Perugia, Italy, 3 Respiratory Unit, Silvestrini Hospital, Perugia, Italy, 4 Sackler Institute of Pulmonary Pharmacology, Pharmaceutical Sciences Research Division, King's College London, London, United Kingdom

* To whom correspondence should be addressed. E-mail: grespa{at}unipg.it.

Rationale: Platelets are essential for pulmonary leukocyte recruitment, airways hyper-responsiveness and bronchial remodeling in animals with allergic inflammation and can be found in broncho-alveolar lavage of sensitized animals. No studies however, have explored the direct migration of platelets to lungs. Objectives: To assess whether platelets migrate into lung parenchyma in response to inhaled allergen in ovalbumin-sensitized mice; to assess the role of the Fc{epsilon}RI receptor in this phenomenon and to evaluate whether platelets from asthmatics, or from sensitized mice, undergo chemotaxis in vitro in response to relevant antigens. Methods: Ovalbumin-sensitized wild-type mice, or FcR{gamma}-/- mice lacking the Fc{epsilon}RI{gamma}, were challenged with aerosolized allergen and lungs analyzed by platelet-specific immuno-histochemistry. In some experiments, mice were depleted of platelets and cross transfused with either wild-type or FcR{gamma}-/- platelets to assess the role of platelet FcR{gamma}-/-. Chemotaxis of platelets from asthmatics or from sensitized mice was studied in vitro. Main Results: Histology of lungs revealed isolated platelets, migrating out of vessels and localizing underneath the airways after allergen challenge in wild-type, but not in FcR{gamma}-/- mice. Platelets from asthmatics and from sensitized wild-type mice, but not from sensitized FcR{gamma}-/- mice, migrated in vitro towards the relevant allergen or an anti-IgE. Platelets from normal mice were found to express Fc{epsilon}RI{gamma} and platelet-bound IgEs were increased in sensitized mice. Conclusions: Platelets migrate extra-vascularly in response to a sensitizing allergen via a mechanism dependent on the interaction between allergen, allergen-specific IgE and the Fc{epsilon}RI and this may allow them to participate directly in allergic tissue inflammation.
Key words: allergen, chemotaxis, Fc{epsilon}RI, IgE, inflammation




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