| First Author | Kung TT | Year | 2004 |
| Journal | Pharmacol Res | Volume | 50 |
| Issue | 6 | Pages | 611-5 |
| PubMed ID | 15501700 | Mgi Jnum | J:309762 |
| Mgi Id | MGI:6708025 | Doi | 10.1016/j.phrs.2004.07.002 |
| Citation | Kung TT, et al. (2004) Tachykinin NK3-receptor deficiency does not inhibit pulmonary eosinophilia in allergic mice. Pharmacol Res 50(6):611-5 |
| abstractText | 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 NK3-receptors on allergen-induced pulmonary inflammation, studies were performed on ovalbumin (OVA) sensitized and challenged mice with genetic disruption of the tachykinin NK3-receptor (NK3-/-). 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 NK3-/- mice and in wild type control mice (NK3+/+). There was no difference in the magnitude of these allergic inflammatory pulmonary responses between NK3-/- and NK3+/+ mice. These results find no role for tachykinin NK3-receptors on the pulmonary eosinophilia and lung damage after antigen challenge in mice. |
