Cutaneous allergic contact dermatitis responses are diminished in mice deficient in neurokinin 1 receptors and augmented by neurokinin 2 receptor blockage

Thomas Scholzen, Martin Steinhoff, Anca Sindrilaru, Agatha Schwarz, Nigel Bunnett, Thomas Luger, Cheryl A Armstrong, John C Ansel

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41 Citations (Scopus)

Abstract

Sensory nerves respond to noxious stimuli by releasing neuropeptides such as the tachykinins substance P (SP) and neurokinin A (NKA). In previous studies, a primary role for SP and its principal neurokinin 1 receptor (NK-1R) was suggested for the initiation and propagation of neurogenic inflammation as part of the inflammatory process in general and also as a component of certain skin disorders such as psoriasis or allergic contact dermatitis (ACD), but the exact role of NKA and the NK-2R in these events is less determined. The availability of mice lacking the NK-1R (NK-1R / ) allowed us to explore whether alterations in the SP/ NK-1R system may dysregulate inflammatory skin responses and to determine the relative contribution of SP and NKA and their respective receptors, NK-1R and NK-2R, on the outcome of an inflammatory response in the skin.
Original languageEnglish
Pages (from-to)1 - 22
Number of pages22
JournalThe FASEB Journal
Volume18
Issue number9
DOIs
Publication statusPublished - 2004

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