Topical acetone treatment induces neurogenic oedema on the sensitized mouse ear: an in vivo study using transient receptor potential vanilloid 1 (TRPV1) receptor knockout mice.Inflamm Res. 2007 Nov; 56(11):459-67.IR
The participation of sensory neurons and transient receptor potential vanilloid 1 (TRPV1) receptors in phorbol 12-myristate 13-acetate (PMA)-induced nerve-sensitizing effect was examined.
MATERIALS AND METHODS
PMA dissolved in acetone and acetone were applied to the ears of TRPV1 receptor knockout and wild-type mice. Different groups of animals received ibuprofen, anti-interleukin-1 beta (IL-1beta) antibody, resiniferatoxin (RTX) or capsaicin pretreatment. Ear thickness, myeloperoxidase activity and IL-1beta content of the ears were determined. Histological evaluation was performed.
PMA exerted potentiating action on contralateral acetone-induced ear oedema, which was inhibited by ibuprofen, topical capsaicin desensitization of the acetone-treated ear as well as by systemic RTX pretreatment. Neither the lack of TRPV1 receptors nor anti-IL-1beta antibody prevented sensitizing effect.
The TRPV1 receptor-independent potentiating action of PMA on contralateral acetone-induced ear oedema is mediated via capsaicin-sensitive afferents and prostanoids are involved. IL-1beta is not essential in this process.