Neuroimmune Interactions in Itch, Pain, & Inflammatory Disease
The SENse Lab aims to understand what drives unpleasant and sometimes deadly immune responses. In conditions like eczema, asthma, and COVID-19, for example, the nervous and immune systems go into overdrive, prompting an exaggerated reaction that can do more harm than good.
Our previous research in atopic dermatitis (AD), also known as eczema, found that skin cells release signaling molecules that activates immune cells and triggers neurons to release inflammatory molecules. Many children with eczema also go on to develop asthma and allergies, a phenomenon known as atopic march. In addition to skin, our lab has found that airway epithelial cells can release the same signaling molecules to activate airway-innervating sensory neurons and promote airway inflammation. |
![]() AD results in barrier dysfunction, which drives production of the cytokines TSLP and CXCL1. CXCL1 can recruit neutrophils, evoking itch through the release of proteases and histamine and inducing CXCL10 expression, which activates sensory neurons. TSLP elicits IL-4 production by basophils, recruiting CD4+ T cells and sensitizing neurons to itch.
Figure adapted from Bautista et al. 2019. Elife. doi: 10.7554/eLife.48448.
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Currently, the SENse Lab aims to elucidate how primary sensory neurons contribute to airway inflammation. In particular, we aim to identify what molecular players mediate airway inflammation and whether such inflammation triggers changes in neuronal activity. Using both in vivo and in vitro methods, we explore new mechanisms of crosstalk between the nervous system and immune system during the development of infectious diseases.