Published ahead of print on October 29, 2004, doi:10.1164/rccm.200406-758OC Am. J. Respir. Crit. Care Med., Volume 171, Number 2, January 2005, 115-120 A more recent version of this article appeared on January 15, 2005
Submitted on June 16, 2004 Brain-derived Neurotrophic Factor in Platelets and Airflow Limitation in AsthmaMarek Lommatzsch1*,1 Department of Pneumology, University of Rostock, Rostock, Germany, 2 Institute of Clinical Chemistry and Pathobiochemistry, University of Rostock, Rostock, Germany, 3 Department of Neurology, Charite, Humboldt University of Berlin, Berlin, Germany * To whom correspondence should be addressed. 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 asthmatics, as compared to 26 age- and sex-matched controls. 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: Neurotrophins, Airway hyperresponsiveness, Peak expiratory flow, Corticosteroids
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