The role of mast cells, interleukin‐13 and transient receptor potential channels in a mouse model of chemical‐induced airway hyperresponsiveness

Abstract

Method On days 1 and 8, wild type C57Bl/6 mice, IL-13, TRP (Transient Receptor Potential) A1, TRPV1 and mast cell deficient mice were dermally sensitized with 1% TDI (toluene-2.4-diisocyanate) or vehicle (acetone/olive oil) on both ears. On day 15, the mice received a single intranasal challenge with 0.1% TDI or vehicle. In a second experiment TDI or vehicle sensitized wild type C57Bl/6 mice received an intraperitoneal injection of the NK1R antagonist RP67580 (1μg/μl) prior to the challenge. Airway reactivity to methacholine, lung inflammation, lymphocyte subpopulations in the draining auricular lymph nodes and total serum IgE were assessed 24h after the challenge.