Published ahead of print on September 16, 2004, doi:10.1164/rccm.200403-385OC Am. J. Respir. Crit. Care Med., Volume 171, Number 1, January 2005, 35-39 A more recent version of this article appeared on January 1, 2005
Submitted on March 24, 2004 Treatment of Cockroach Allergen Asthma Model with Imatinib Attenuates Airway ResponsesAaron A Berlin1 and Nicholas W Lukacs1*1 Department of Pathology, University of Michigan Medical School, Ann Arbor, MI, USA * To whom correspondence should be addressed. E-mail: nlukacs{at}umich.edu.
In the present study it was determined whether a pharmacological approach to blocking receptor tyrosine kinase-mediated activation during allergic airway responses could be beneficial. In order to examine these responses, allergic mice were given a single oral dose of imatinib at clinically relevant concentrations, ranging from 0.05 to 50 mg/kg, by oral gavages just prior to allergen challenge. The reduction in the allergen-induced responses was significant and centered on reducing overall inflammation as well as pulmonary cytokine levels. In particular, the treatment of the mice with Imatinib significantly attenuated airway hyperreactivity, peribronchial eosinophil accumulation and significantly reduced Th2 cytokines, IL-4 and IL-13. In addition, chemokines previously associated with allergen-induced pulmonary disease, CCL2, CCL5, and CCL6, were significantly reduced in the lungs of the Imatinib treated animals. Together, these data demonstrate that the pharmacological inhibitor, Imatinib, may provide a clinically attractive therapy for allergic, asthmatic responses. Key words: asthma, airway hyperreactivity, inflammation, eosinophils
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