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Impaired IL‐1 β ‐induced neutrophil accumulation in tachykinin NK 1 receptor knockout mice
Author(s) -
Ahluwalia Amrita,
De Felipe Carmen,
O'Brien John,
Hunt Stephen P.,
Perretti Mauro
Publication year - 1998
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1038/sj.bjp.0701978
Subject(s) - receptor , tachykinin receptor , substance p , knockout mouse , inflammation , endocrinology , medicine , cytokine , immunology , chemotaxis , chemistry , biology , neuropeptide
Tachykinin NK 1 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‐1β (IL‐1β, 10 ng into the air‐pouch) is altered in NK 1 receptor knockout mice compared to wild type controls. Air‐pouches were washed following a 4 h IL‐1β treatment, the wash collected and neutrophil number estimated using a Neubauer haemocytometer. The response to IL‐1β was significantly attenuated in NK 1 receptor +/− (40% reduction) and −/− mice (62% reduction) compared to wild type controls (+/+), whilst the response to cytokine‐induced neutrophil chemoattractant (CINC, 0.3 μg) was unaffected. The response to substance P (7.5 nmol) was attenuated by approximately 50% in both NK 1 receptor +/− and −/− mice compared to wild type controls. In conclusion NK 1 receptors play a significant role in the cellular response to IL‐1β in a model of inflammation. British Journal of Pharmacology (1998) 124 , 1013–1015; doi: 10.1038/sj.bjp.0701978