title: Inflammatory stimuli acutely modulate peripheral taste function.
abstract: 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 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, 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.
authors.affiliation: Department of Neuroscience and Regenerative Medicine, Medical College of Georgia at Augusta University, Augusta, Georgia; and Graduate Program in Molecular Medicine, Medical College of Georgia at Augusta University, Augusta, Georgia.
authors.forename: Devaki
authors.initials: D
authors.lastname: Kumarhia
authors.affiliation: Department of Neuroscience and Regenerative Medicine, Medical College of Georgia at Augusta University, Augusta, Georgia; and.
authors.forename: Lianying
authors.initials: L
authors.lastname: He
authors.affiliation: Department of Neuroscience and Regenerative Medicine, Medical College of Georgia at Augusta University, Augusta, Georgia; and lmccluskey@augusta.edu.
authors.forename: Lynnette Phillips
authors.initials: LP
authors.lastname: McCluskey
mesh_terms: D000584:Amiloride / Q000494:pharmacology; D018712:Analgesics, Non-Narcotic / Q000494:pharmacology; D000704:Analysis of Variance; D000818:Animals; D001835:Body Weight / Q000187:drug effects; D002211:Capsaicin / Q000031:analogs & derivatives / Q000494:pharmacology; D002814:Chorda Tympani Nerve / Q000000981:diagnostic imaging / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D062686:Epithelial Sodium Channel Blockers / Q000494:pharmacology; D005260:Female; D007839:Functional Laterality / Q000187:drug effects; D015850:Interleukin-6 / Q000494:pharmacology*; D008070:Lipopolysaccharides / Q000494:pharmacology; D011803:Quinine / Q000494:pharmacology; D051381:Rats; D011984:Sensory Receptor Cells / Q000187:drug effects; D012964:Sodium / Q000378:metabolism*; D019346:Sodium Acetate / Q000494:pharmacology; D012965:Sodium Chloride / Q000494:pharmacology; D013650:Taste Buds / Q000000981:diagnostic imaging / Q000187:drug effects*; D015898:Tomography Scanners, X-Ray Computed; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
chemical_list: D018712:Analgesics, Non-Narcotic; D062686:Epithelial Sodium Channel Blockers; D015850:Interleukin-6; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D012965:Sodium Chloride; D019346:Sodium Acetate; D000584:Amiloride; D012964:Sodium; D011803:Quinine; C071423:capsazepine; D002211:Capsaicin
keywords: epithelial sodium channel; interleukin-1β; neuroimmunology; taste bud; tumor necrosis factor-α