Skin tastes bitter molecules through sensory receptors – The hop bitterness that calms your skin senses
ANGELA ROCA1*, MIGUEL PÉREZ-ASO1, BLANCA MARTÍNEZ-TEIPEL1, JORDI BOSCH1, MERCÈ TENA-CAMPOS2, PERE GARRIGA2
*Corresponding author
1. Provital S.A.U., Barcelona, Spain
2. Grup de Biotecnologia Molecular i Industria, Universitat Politècnica de Catalunya, Terrassa, Spain
Abstract
The skin is the largest sensory organ in our body whose function is the protection from harmful environmental stimuli. Recently, bitter taste receptors have been described in the skin as well as in other extra-oral tissues. Here we demonstrate the presence of bitter taste receptors both in fibroblasts and keratinocytes and their possible role in the immune system homeostasis. Besides, a hop ingredient activates skin bitter taste receptors to boost the immune system, to protect the skin from external aggressions reporting beneficial effects on allergic or reactive skin and calming the cutaneous discomfort such as itching and stinging sensations.
INTRODUCTION
The skin is a complex sensory system, reacting to the environment through an integrated network of cell receptors. This sensory system can detect changes in pressure, temperature, vibration, and tactile sensations(1). But over the last years, other chemoreceptors, G-protein-Coupled Receptors (GPCRs) related to our senses, have been described in the skin such as opsins, olfactory and taste receptors, opening a new window to target novel mechanisms for the cosmetic industry.
Human bitter taste perception is mediated by 25 bitter taste receptors (T2Rs) which are GPCRs located in the taste buds of the tongue, where they initiate signal transduction (2) after activation by diverse bitter compounds. Bitter tastants binding to the receptor induces activation of the taste-specific heterotrimeric G-protein gustducin. Once activated, Gα-gustducin initiates a signalling cascade to generate inositol-1,4,5-triphosphate (IP3) and diacylglycerol (DAG). This IP3 activates calcium release and the elevated Ca2+ opens transient receptor potential cation channel member 5 (TRPM5) that leads to membrane depolarization (Figure 1) and subseq ...
