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- Modulation of visceral sensory nerves by inflammation
- Regulation of cough reflex
Sensory nerves gather information about the tissue. Our research focus on specific phenotype of visceral sensory nerves, termed nociceptive, that detect stimuli associated with impeding or actual tissue damage. Nociceptors trigger defensive reflexes and/or sensations of discomfort and pain. For example, nociceptors initiate cough, sneezing, nasal itching, bronchoconstriction and mucus hypersecretion in respiratory system, and pain and hypersecretion in gastrointestinal system. Increase in nociceptive activity contributes significantly to the pathogenesis of respiratory and gastrointestinal diseases and their symptoms. Importantly, inflammation profoundly alters properties of nociceptive nerves per se leading in general to exaggerated nociceptive responsiveness. Our studies center on this aspect of visceral nociception in allergic and non-allergic inflammatin. We carry out electrophysiological and anatomical studies in isolated tissues and reflex studies in animal models.
1) Activation and regulation of excitability of visceral nociceptors in inflammation. Ionic mechanisms by which inflammatory mediators excite and modulate nociceptors. We are particularly interested in acid (currently evaluate role of the TRP and ASIC receptors) and mediators that act via G-protein coupled receptors (GPCRs): bradykinin, adenosine and histamine (role of the TRP receptors and certain chloride channels).
2) Visceral sensory plasticity. Mechanisms of long-term alteration of nociceptive phenotypes by inflammatory mediators.
3) Nociceptive modulation of cough reflex. Mechanisms of cough exaggeration by nasal and esophageal nociceptors. These mechanisms operate in chronic cough.