Description (provided by applicant): Peripheral nerve injury has effects that extend beyond damaged neurons. However, the impact of injury on neighboring sensory fields is not well understood. We propose that immune cells, or leukocytes, mediate changes in taste function. Macrophages respond to nerve injury, and extend to uninjured regions of the tongue. These leukocytes are predictive of normal neural taste responses. Neutrophils are also part of the immune response to injury, but they appear to have a negative effect on taste function. Neural injury alters sodium transduction in taste receptor cells, suggesting that the epithelial sodium channel (ENaC) is the site of functional plasticity. We will test the following hypotheses: (1) Neutrophils are the initial immune responders to gustatory nerve injury, and they induce deficits in taste function; (2) Nerve injury and leukocytes modulate ENaC expression and/or function; and (3) IL-12, a proinflammatory cytokine, maintains normal taste function after injury by promoting a balanced immune response. Resolution of these hypotheses will increase our understanding of dynamic immune responses to neural injury and their beneficial and harmful effects on sensory receptor cells.
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