Tachykinin NK 3-receptor deficiency does not inhibit pulmonary eosinophilia in allergic mice

Abstract

Tachykinins are important in the development of pulmonary inflammation in mice but the tachykinin receptor subtype mediating this response has not been defined. To elucidate the role of tachykinin NK 3-receptors on allergen-induced pulmonary inflammation, studies were performed on ovalbumin (OVA) sensitized and challenged mice with genetic disruption of the tachykinin NK 3-receptor (NK 3 −/−). Aerosol OVA (0.5%) challenge produced eosinophil influx into the bronchoalveolar lavage fluid and lung tissue, goblet cell hyperplasia and damage to the airway epithelium of both NK 3 −/− mice and in wild type control mice (NK 3 +/+). There was no difference in the magnitude of these allergic inflammatory pulmonary responses between NK 3 −/− and NK 3 +/+ mice. These results find no role for tachykinin NK 3-receptors on the pulmonary eosinophilia and lung damage after antigen challenge in mice.