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 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.
journal_name
Pharmacol Resjournal_title
Pharmacological researchauthors
Kung TT,Crawley Y,Jones H,Luo B,Gilchrest H,Greenfeder S,Anthes JC,Lira S,Wiekowski M,Cook DN,Hey JA,Egan RW,Chapman RWdoi
10.1016/j.phrs.2004.07.002keywords:
subject
Has Abstractpub_date
2004-12-01 00:00:00pages
611-5issue
6eissn
1043-6618issn
1096-1186pii
S1043-6618(04)00177-Xjournal_volume
50pub_type
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