Abstract
TRPA1 has been proposed to be associated with diverse sensory allergic reactions, including thermal (cold) nociception, hearing and allergic inflammatory conditions. Some naturally occurring compounds are known to activate TRPA1 by forming a Michael addition product with a cysteine residue of TRPA1 through covalent protein modification and, in consequence, to cause allergic reactions. The anti-allergic property of TRPA1 agonists may be due to the activation and subsequent desensitization of TRPA1 expressed in sensory neurons. In this review, naturally occurring TRPA1 antagonists, such as camphor, 1,8-cineole, menthol, borneol, fenchyl alcohol and 2-methylisoborneol, and TRPA1 agonists, including thymol, carvacrol, 1’S-1’- acetoxychavicol acetate, cinnamaldehyde, α-n-hexyl cinnamic aldehyde and thymoquinone as well as isothiocyanates and sulfides are discussed.
Highlights
Allergies have been known as hypersensitivity disorders of the immune system since the beginning of the 19th century, and the concept of hay fever was described around same period
Biological activities of menthol associated with allergy were demonstrated as menthol-rich peppermint oil and menthol itself were seen to suppress passive cutaneous anaphylaxis reaction (PCA) mediated by IgE antibody in guinea pigs and menthol reduced antigeninduced histamine release from rat peritoneal mast cells [52]
There are two groups of naturally occurring flavor and fragrance chemicals associated with TRPA1: one group comprises the antagonists, such as camphor, 1,8-cineole, menthol, borneol and fenchyl alcohol; and the other group is the agonists, such as thymol, carvacrol, 1’S-1’-acetoxychavicol acetate, cinnamaldehyde, thymoquinone and isothiocyanates
Summary
Allergies have been known as hypersensitivity disorders of the immune system since the beginning of the 19th century, and the concept of hay fever was described around same period. These phenomena suggest the anti-allergic activities induced by camphor are due to the desensitization of TRPV1 and the blockage of TRPA1 [24,29].
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