Impaired IL-1β-induced neutrophil accumulation in tachykinin NK1 receptor knockout mice

被引:48
作者
Ahluwalia, AA [1 ]
De Felipe, C
O'Brien, J
Hunt, SP
Perretti, M
机构
[1] UCL, Rayne Inst, Ctr Clin Pharmacol, Cruciform Project, London WC1E 6JJ, England
[2] Univ Alcala de Henares, Fac Med, Inst Neurociencias, Madrid 28871, Spain
[3] MRC, Mol Biol Lab, Div Neurobiol, Cambridge CB2 2QH, England
[4] William Harvey Res Inst, Dept Biochem Pharmacol, London EC1M 6BQ, England
关键词
substance P; inflammation; sensory C-fibre; chemokine;
D O I
10.1038/sj.bjp.0701978
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Tachykinin NK1 receptors play an important role in the development of neurogenic inflammatory responses. We have used the murine air-pouch model to investigate whether the neurogenic component of the cellular inflammatory response to interleukin-1 beta (IL-1 beta, 10 ng into the air-pouch) is altered in NK1 receptor knockout mice compared to wild type controls. Air-pouches were washed following a 4 h IL-1 beta treatment, the wash collected and neutrophil number estimated using a Neubauer haemocytometer. The response to IL-IP was significantly attenuated in NK1 receptor +/- (40% reduction) and -/- mice (62% reduction) compared to wild type controls (+/+), whilst the response to cytokine-induced neutrophil chemoattractant (CINC, 0.3 mu g) was unaffected. The response to substance P (7.5 nmol) was attenuated by approximately 50% in both NK1 receptor +/- and -/- mice compared to wild type controls. In conclusion NK1 receptors play a significant role in the cellular response to IL-1 beta in a model of inflammation.
引用
收藏
页码:1013 / 1015
页数:3
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