Neural-immune crosstalk in itch and skin inflammation

Pruriceptors are the specific subsets of sensory neurons that produce itch. Atopic dermatitis (AD) is a chronic skin inflammatory disease that is characterized by itchy and inflamed lesions. Chronic itch is difficult to treat. One of the goals in our lab is to define neuroimmune mechanisms that drive itch and skin inflammation. Pruciceptor neurons express receptors for specific immune derived factors, including lipid mediators and cytokines. We have recently found that the cysteinyl leukotriene LTC4 activates itch in pruriceptors through its receptor Cysltr2, and that this drives itch in a mouse model of AD. We are now investigating how microbes in the skin could also impact itch. 95% of AD lesions are colonized by Staphylococcus aureus, a major human pathogen that could drive neural activation and itch. We are interested in determining how S. aureus could drive itch and inflammation in AD.

Publications on this topic:

1. Voisin T, Perner C, Messou MA, Shiers S, Kanaoka Y, Price TJ, Sokol CL, Bankova LG, Austen KF*, Chiu IM*. The CysLT2R receptor mediates leukotriene C4-driven acute and chronic itch. Proc. Natl. Acad. Sci. USA 2021 Mar 30;118(13)e2022087188. *Co-corresponding authors. PMCID: PMC8020753.  PDF