Tachykinin NK3-receptor deficiency does not inhibit pulmonary eosinophilia in allergic mice

被引：39

作者：

Kung, TT ^{[1
]}

Crawley, Y ^{[1
]}

Jones, H ^{[1
]}

Luo, B ^{[1
]}

Gilchrest, H ^{[1
]}

Greenfeder, S ^{[1
]}

Anthes, JC ^{[1
]}

Lira, S ^{[1
]}

Wiekowski, M ^{[1
]}

Cook, DN ^{[1
]}

Hey, JA ^{[1
]}

Egan, RW ^{[1
]}

Chapman, RW ^{[1
]}

机构：

[1] Schering Plough Res Inst, Dept Allergy & Immunol, Kenilworth, NJ 07033 USA

来源：

PHARMACOLOGICAL RESEARCH | 2004年 / 50卷 / 06期

关键词：

tachykinin NK3-receptor; allergen; eosinophil; mice;

D O I：

10.1016/j.phrs.2004.07.002

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

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 and NK3+/+ mice. These results find no role for tachykinin NK3-receptors on allergic inflammatory pulmonary responses between NK3-/- 3 the pulmonary eosinophilia and lung damage after antigen challenge in mice. (C) 2004 Elsevier Ltd. All rights reserved.

引用

页码：611 / 615

页数：5

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