Pain and itch sensations in the skin are initiated by activation of a complex signaling network involving somatosensory neurons and numerous resident skin cells. Tissue damage and inflammation can produce a localized or systemic sensitization of our senses of pain and itch to facilitate our detection of noxious environment. Although acute pain and itch protect us from further damage, persistent pain and itch are two major clinical issues associated with many disease conditions and represent a significant unmet medical need for patients around the globe. Recent exciting findings have shown that distinct cellular and molecular mechanisms are involved in the pathogenesis of itch and pain although they use similar neural pathways.
The Hu laboratory has taken a multidisciplinary approach to understand the cellular and molecular mechanisms of pain and itch focusing on transient receptor potential (TRP) channels in the skin and primary sensory neurons under physiological and pathophysiological conditions. We use electrophysiological and pharmacological approaches in combination with molecular biology, genetics and behavioral methods to gain fundamental insights into the roles of membrane receptors and ion channels in epidermal keratinocytes, cutaneous immune cells (macrophages, dendritic cells, and lymphocytes), and primary sensory neurons. Knowledge of the underlying mechanisms of pain and itch is the key for a better understanding of these two phenomena and will lead to new rationale-based treatment approaches by selectively targeting specific itch and pain signaling pathways.