We have investigated the effect of IL-1 � on histamine H 1-receptor (H 1R)-mediated inositol phosphate (IP) accumulation in human airway smooth muscle cells (HASMC) and on histamine-induced contraction of human bronchial rings. Stimulation of HASMC for 24 h with IL-1 � resulted in significant loss of histamine-induced IP formation, which was associated with a reduction of histamineinduced contraction of IL-1�-treated human bronchial rings. An inhibitor of NF-�B activation, pyrrolidine dithiocarbamate, and a p38 MAPK inhibitor, blocked the IL-1�-induced H 1R desensitization, whereas anisomycin, an SAPK/JNK and p38 MAPK activator, mimicked the effect of IL-1�. IL-1 � has been demonstrated to induce cox-2 expression and PGE 2 synthesis. In our study, indomethacin a cox antagonist, completely inhibited the effect of IL-1 � on H 1R, whereas exogenously added PGE 2 was able to desensitize H 1R. Furthermore, H-89, a selective PKA inhibitor, antagonized the effec
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