TY - JOUR
T1 - Inflammatory stimuli acutely modulate peripheral taste function
AU - Kumarhia, Devaki
AU - He, Lianying
AU - McCluskey, Lynnette Phillips
N1 - Publisher Copyright:
© 2016 the American Physiological Society.
PY - 2016/6/1
Y1 - 2016/6/1
N2 - Inflammation-mediated changes in taste perception can affect health outcomes in patients, but little is known about the underlying mechanisms. In the present 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 amiloridesensitive 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, although 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 and 2 h after LPS treatment. Low, normally preferred concentrations of NaCl and sodium acetate elicited high response magnitudes. Consistent with this outcome, codelivery of IL-1β and TNF-α 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.
AB - Inflammation-mediated changes in taste perception can affect health outcomes in patients, but little is known about the underlying mechanisms. In the present 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 amiloridesensitive 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, although 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 and 2 h after LPS treatment. Low, normally preferred concentrations of NaCl and sodium acetate elicited high response magnitudes. Consistent with this outcome, codelivery of IL-1β and TNF-α 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.
KW - Epithelial sodium channel
KW - Interleukin-1β
KW - Neuroimmunology
KW - Taste bud
KW - Tumor necrosis factor-α
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U2 - 10.1152/jn.01104.2015
DO - 10.1152/jn.01104.2015
M3 - Article
C2 - 27009163
AN - SCOPUS:84984846840
SN - 0022-3077
VL - 115
SP - 2964
EP - 2975
JO - Journal of Neurophysiology
JF - Journal of Neurophysiology
IS - 6
ER -