Impaired IL-1β-induced neutrophil accumulation in tachykinin NK1 receptor knockout mice
Impaired IL-1β-induced neutrophil accumulation in tachykinin NK1 receptor knockout mice
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DOI：
10.1038/sj.bjp.0701978
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发表时间：
1998-07-01
影响因子：
7.3
通讯作者：
Perretti, M
中科院分区：
文献类型：
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作者：
Ahluwalia, AA;De Felipe, C;Perretti, M
速激肽NK1受体在神经源性炎症反应的发生中起重要作用。我们使用小鼠气囊模型来研究与野生型对照相比，NK1受体基因敲除小鼠对白介素1β(IL-1β，10 ng进入气囊)的细胞炎症反应的神经源性成分是否发生了改变。在IL-1β处理4h后，清洗气囊，收集洗液并用Neubauer血细胞计数仪估计中性粒细胞数量。与野生型对照(+/+)相比，NK1受体+/-(减少40%)和-/-小鼠(减少62%)对IL-IP的反应显著减弱，而对细胞因子诱导的中性粒细胞趋化因子(CINC，0.3mU/g)的反应不受影响。与野生型对照相比，NK1受体+/-和-/-小鼠对P物质(7.5nmoL)的反应都减弱了约50%。总之，在炎症模型中，NK1受体在细胞对IL-1β的反应中起着重要作用。
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.