Regulation of bitter taste responses by tumor necrosis factor.
Regulation of bitter taste responses by tumor necrosis factor.
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DOI：
10.1016/j.bbi.2015.04.001
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发表时间：
2015-10
期刊：
影响因子：
--
通讯作者：
Wang H
中科院分区：
文献类型：
--
作者：
Feng P;Jyotaki M;Kim A;Chai J;Simon N;Zhou M;Bachmanov AA;Huang L;Wang H
炎性细胞因子是代谢和食物摄入的重要调节因子。在细菌和病毒感染期间，炎症细胞因子的过度产生导致厌食症和食物摄入量减少。然而，目前还不清楚是否有任何炎症细胞因子参与味觉感受的调节，味觉感受是控制食物摄入的感觉机制。以前，我们表明，肿瘤坏死因子（TNF），一种有效的促炎细胞因子，优先表达在味蕾细胞的一个子集。味觉细胞中的TNF水平可进一步由炎症刺激诱导。为了研究TNF是否在调节味觉反应中起作用，在这项研究中，我们对TNF敲除小鼠进行了味觉行为测试和味觉神经记录。行为测试表明，TNF缺陷小鼠对苦味化合物奎宁的敏感性明显低于野生型小鼠，而它们对甜味、鲜味、咸味和酸味化合物的反应与野生型对照小鼠相当。此外，神经记录实验表明，TNF敲除小鼠的鼓索神经对苦味化合物的反应比野生型小鼠低得多。鼓索神经对甜味、鲜味、咸味和酸味化合物的反应在TNF敲除小鼠和野生型小鼠之间是相似的，这与行为测试的结果一致。我们进一步表明，味蕾细胞表达两种已知的TNF受体TNFR 1和TNFR 2，因此是TNF的潜在靶点。总之，我们的研究结果表明，TNF信号优先调节苦味反应。这种机制可能导致味觉功能障碍，特别是味觉扭曲，与感染和一些慢性炎症性疾病有关。
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.