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Regulation of bitter taste responses by tumor necrosis factor
Journal article   Open access   Peer reviewed

Regulation of bitter taste responses by tumor necrosis factor

Pu Feng, Masafumi Jyotaki, Agnes Kim, Jinghua Chai, Nirvine Simon, Minliang Zhou, Alexander A Bachmanov, Liquan Huang, Hong Wang and Aimee Yuka W Kim
Brain, behavior, and immunity, v 49, pp 32-42
Oct 2015
PMID: 25911043
url
https://doi.org/10.1016/j.bbi.2015.04.001View
Accepted (AM)Open Access (Publisher-Specific) Open

Abstract

Animals Behavior, Animal - physiology Chorda Tympani Nerve - physiology Citric Acid Female Inosine Monophosphate Male Mice Mice, Inbred C57BL Mice, Knockout Quinine Saccharin Sodium Chloride Sodium Glutamate Taste - physiology Taste Buds - cytology Taste Buds - metabolism Taste Perception - physiology Tumor Necrosis Factor-alpha - genetics Tumor Necrosis Factor-alpha - metabolism Tumor Necrosis Factor-alpha - physiology
Inflammatory cytokines are important regulators of metabolism and food intake. Over production of inflammatory cytokines during bacterial and viral infections leads to anorexia and reduced food intake. However, it remains unclear whether any inflammatory cytokines are involved in the regulation of taste reception, the sensory mechanism governing food intake. Previously, we showed that tumor necrosis factor (TNF), a potent proinflammatory cytokine, is preferentially expressed in a subset of taste bud cells. The level of TNF in taste cells can be further induced by inflammatory stimuli. To investigate whether TNF plays a role in regulating taste responses, in this study, we performed taste behavioral tests and gustatory nerve recordings in TNF knockout mice. Behavioral tests showed that TNF-deficient mice are significantly less sensitive to the bitter compound quinine than wild-type mice, while their responses to sweet, umami, salty, and sour compounds are comparable to those of wild-type controls. Furthermore, nerve recording experiments showed that the chorda tympani nerve in TNF knockout mice is much less responsive to bitter compounds than that in wild-type mice. Chorda tympani nerve responses to sweet, umami, salty, and sour compounds are similar between TNF knockout and wild-type mice, consistent with the results from behavioral tests. We further showed that taste bud cells express the two known TNF receptors TNFR1 and TNFR2 and, therefore, are potential targets of TNF. Together, our results suggest that TNF signaling preferentially modulates bitter taste responses. This mechanism may contribute to taste dysfunction, particularly taste distortion, associated with infections and some chronic inflammatory diseases.

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Web of Science research areas
Immunology
Neurosciences
Psychiatry
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