Bitter Taste Responses Tumor Necrosis Factor

Bitter Taste Responses and Tumor Necrosis Factor

Bitter Taste and TNF

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.

Taste is the sensory system for detecting nutrients and potentially harmful substances in food and drink and, therefore, plays important roles in guiding food intake. Among the five basic taste modalities, sweet and umami tastes detect sugars and amino acids, respectively, and are generally preferred.

Bitter taste recognizes toxins and noxious compounds and elicits avoidance behavior. Acids and salts are detected by sour and salt taste mechanisms. Recent research has made rapid progress in understanding taste receptors and signaling pathways.

Many diseases with underlying inflammation, such as infections and autoimmune ailments, are associated with taste alterations. Taste alterations can occur as taste loss (lacking or reduced taste reception) or taste distortion (e.g. persistent bitter or metallic taste in the mouth). In animal models, induced inflammation has been shown to affect taste responses and taste bud structur.

Whether inflammatory cytokines contribute to taste reception or regulation is poorly understood. Previous studies have found that several inflammation-associated cytokines are preferentially expressed in taste bud cells compared to nontaste lingual epithelial cells, suggesting that these cytokines may have special functions in the peripheral taste system.

TNF is specifically expressed in a subset of taste bud cells even in healthy mice. Immunocolocalization experiments showed that TNF is colocalized with the sweet and umami taste receptor subunit T1R3, indicating that TNF is expressed specifically in the sweet and umami taste bud cell.

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.

In Tthe Brain, Behavior, and Immunity study the investigators used TNF knockout mice and their wild-type controls to investigate the role of TNF in the taste system. They conducted gustatory nerve recording and taste behavioral testing using these mice.

The authors found that TNF-deficient mice are significantly less responsive to bitter compounds than control mice, whereas their responses to sweet, umami, sour, and salty compounds did not differ significantly from those of control mice.

We further showed that taste bud cells express the two known TNF receptors TNFR1 and TNFR2 and, therefore, are potential targets of TNF.

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.

Source: Brain Behav Immun. 2015 Apr 21. pii: S0889-1591(15)00086-0. doi: 10.1016/j.bbi.2015.04.001. [Epub ahead of print]

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