Iodine antiseptics exhibit superior antimicrobial efficacy and do not cause acquired microbial resistance. However, they are underused in comparison with antibiotics in infection treatments, partly because of their adverse effects such as pain and allergy. The cause of these noxious effects is not fully understood, and no specific molecular targets or mechanisms have been discovered. In this study, we show that iodine antiseptics cause pain and promote allergic contact dermatitis in mouse models, and iodine stimulates a subset of sensory neurons that express TRPA1 and TRPV1 channels. In vivo pharmacological inhibition or genetic ablation of these channels indicates that TRPA1 plays a major role in iodine antiseptics‐induced pain and the adjuvant effect of iodine antiseptics on allergic contact dermatitis and that TRPV1 is also involved. We further demonstrate that iodine activates TRPA1 through a redox mechanism but has no direct effects on TRPV1. Our study improves the understanding of the adverse effects of iodine antiseptics and suggests a means to minimize their side effects through local inhibition of TRPA1 and TRPV1 channels.
This report identifies the cation channel TRPA1 as an endogenous molecular target of iodine in mammals. The iodine‐dependent activation of TRPA1 and also TRPV1 is associated with major iodine antiseptics‐induced adverse reactions such as pain and cutaneous allergy.
TRPA1 is a major mediator of iodine antiseptics‐induced pain.
Iodine in the PVP‐I iodophor promotes contact hypersensitivity mainly through a direct TRPA1‐dependent mechanism.
Also TRPV1 plays a role in the adverse effects of iodine antiseptics.
EMBO Reports (2016) 17: 1422–1430
- Received March 9, 2016.
- Revision received July 26, 2016.
- Accepted August 1, 2016.
- © 2016 The Authors