A new study by Pu Feng and colleagues from the Monell Chemical Senses Center, Philadelphia, USA, published in Brain, Behavior, and Immunity indicates that tumor necrosis factor(TNF)-α, a major pro-inflammatory cytokine is involved in the regulation of bitter taste reception.
Whether inflammatory cytokines contribute to taste reception or regulation is poorly understood.
TNF is known to be part of the cause of ‘sickness behavior’ including fatigue, malaise, depression, and anorexia and to induce significant reduction in food intake both in rodents and in humans. Previous research also indicates that some pro-inflammatory cytokines are expressed in taste bud cells but not in nontaste lingual epithelial cells.
The Brain, Behavior, and Immunity study reports that TNF-deficient mice are less responsive to bitter compounds than control mice. The authors of this study suggested that during physiological conditions, TNF preferentially sensitizes bitter taste responses. However, under inflammatory conditions, when the TNF production is enhanced in taste buds, TNF may affect other types of taste cells in addition to its effect on bitter cells.
According to the authors these phenomena and mechanisms may contribute to taste dysfunction associated with some infections or inflammatory conditions.