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Published ahead of print on October 29, 2004, doi:10.1164/rccm.200406-758OC
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American Journal of Respiratory and Critical Care Medicine Vol 171. pp. 115-120, (2005)
© 2005 American Thoracic Society
doi: 10.1164/rccm.200406-758OC

Original Article

Brain-derived Neurotrophic Factor in Platelets and Airflow Limitation in Asthma

Marek Lommatzsch, Katharina Schloetcke, Jens Klotz, Katharina Schuhbaeck, Doerte Zingler, Christiana Zingler, Olaf Schulte-Herbrüggen, Hartmut Gill, Peter Schuff-Werner and Johann Christian Virchow

Department of Pneumology and Institute of Clinical Chemistry and Pathobiochemistry, University of Rostock, Rostock; Department of Neurology, Charité, Berlin, Germany

Correspondence and requests for reprints should be addressed to Marek Lommatzsch, M.D., Abteilung für Pneumologie, Klinik und Poliklinik für Innere Medizin, Universität Rostock, Ernst-Heydemann-Str. 6, Rostock 18057, Germany. E-mail: marek.lommatzsch{at}med.uni-rostock.de

Brain-derived neurotrophic factor (BDNF), a key mediator of neuronal plasticity, contributes to airway obstruction and hyperresponsiveness in a model of allergic asthma. BDNF is stored in human platelets and circulates in human plasma, but the significance of BDNF in this compartment is poorly understood. We investigated the relationship between platelet and plasma BDNF levels and pulmonary function in a cohort of 26 adult patients with recently diagnosed allergic asthma. BDNF levels in serum, platelets, and plasma were significantly increased in participants with asthma, as compared with 26 age- and sex-matched control subjects. In steroid-naive patients, but not in patients using inhaled corticosteroids, enhanced platelet BDNF levels correlated with parameters of airway obstruction and airway hyperresponsiveness to histamine. Experiments with activated peripheral blood mononuclear cells revealed that corticosteroids such as fluticasone effectively suppress BDNF secretion. In conclusion, we demonstrate that enhanced platelet BDNF is associated with airflow limitation and airway hyperresponsiveness in asthma. In addition, we provide evidence that corticosteroids suppress BDNF production by activated immune cells.

Key Words: airway hyperresponsiveness • corticosteroids • neurotrophins • peak expiratory flow




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