Inflammation-mediated changes in taste perception can affect health outcomes in patients, but little is known about underlying mechanisms. In the current work, we hypothesized that proinflammatory cytokines directly modulate Na+ transport in taste buds. To test this, we measured acute changes in Na+ flux in polarized fungiform taste buds loaded with a Na+ indicator dye. IL-1β elicited an amiloride-sensitive increase in Na+ transport in taste buds. In contrast, TNF-α dramatically and reversibly decreased Na+ flux in polarized taste buds via amiloride-sensitive and amiloride-insensitive Na+ transport systems. The speed and partial amiloride-sensitivity of these changes in Na+ flux indicate that IL-1β and TNF-α modulate epithelial Na+ channel (ENaC) function. A portion of the TNF-mediated decrease in Na+ flux is also blocked by the TRPV1 antagonist, capsazepine, though TNF-α further reduced Na+ transport independently of both amiloride and capsazepine. We also assessed taste function in vivo in a model of infection and inflammation that elevates these and additional cytokines. In rats administered systemic lipopolysaccharide (LPS), CT responses to Na+ were significantly elevated between 1-2-hr after LPS treatment. Low, normally preferred concentrations of NaCl and sodium acetate (NaAc) elicited high response magnitudes. Consistent with this outcome, co-delivery of IL-1β and TNF-β enhanced Na+ flux in polarized taste buds. These results demonstrate that inflammation elicits swift changes in Na+ taste function, which may limit salt consumption during illness.
- taste bud
- Copyright © 2015, Journal of Neurophysiology