Ingestion of bacterial lipopolysaccharide inhibits peripheral taste responses to sucrose in mice.

Ingestion of bacterial lipopolysaccharide inhibits peripheral taste responses to sucrose in mice.
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DOI:
10.1016/j.neuroscience.2013.10.072
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发表时间:
2014-01-31
期刊:
影响因子:
3.3
通讯作者:
McCluskey LP
McCluskey LP
中科院分区:
医学3区
文献类型:
--
作者:
Zhu X;He L;McCluskey LP

文献摘要

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味觉系统的一个基本作用是区分有营养的食物和有毒的食物。然而,目前尚不清楚可能污染食物和水的细菌病原体是否会调节味觉输入到大脑的传输。我们假设,外源性,细菌衍生的脂多糖(LPS),调制味觉刺激的神经反应。神经生理反应鼓索神经,支配味觉细胞的前舌,是不变的急性暴露于LPS。相反,在一个单一的过夜期间饮用LPS的小鼠中,对蔗糖的神经反应被选择性地抑制。在LPS摄入后7天出现蔗糖敏感性降低,与Tas1r2和Tas1r3转录物的舌表达降低平行,Tas1r2和Tas1r3转录物被翻译成T1R2+T1R3亚基形成甜味受体。LPS消耗后14天,Tas1 r2和Tas1 r3 mRNA表达水平和对蔗糖的神经反应得到恢复。摄入LPS,而不是与味觉受体细胞接触,似乎是必要的,以抑制蔗糖反应。此外,缺乏LPS的Toll样受体(TLR)4的小鼠对LPS消耗后的神经生理学变化具有抗性。这些发现表明,在一个单一的时期内摄入LPS特异性和短暂抑制神经反应蔗糖。我们认为,LPS饮用启动TLR4依赖的激素信号,下调味蕾中的甜味受体基因。甜味信号的延迟抑制可能会影响食物选择以及胃肠道细菌和肥胖之间复杂的相互作用。
A fundamental role of the taste system is to discriminate between nutritive and toxic foods. However, it is unknown whether bacterial pathogens that might contaminate food and water modulate the transmission of taste input to the brain. We hypothesized that exogenous, bacterially-derived lipopolysaccharide (LPS), modulates neural responses to taste stimuli. Neurophysiological responses from the chorda tympani nerve, which innervates taste cells on the anterior tongue, were unchanged by acute exposure to LPS. Instead, neural responses to sucrose were selectively inhibited in mice that drank LPS during a single overnight period. Decreased sucrose sensitivity appeared 7 days after LPS ingestion, in parallel with decreased lingual expression of Tas1r2 and Tas1r3 transcripts, which are translated to T1R2+T1R3 subunits forming the sweet taste receptor. Tas1r2 and Tas1r3 mRNA expression levels and neural responses to sucrose were restored by 14 days after LPS consumption. Ingestion of LPS, rather than contact with taste receptor cells, appears to be necessary to suppress sucrose responses. Furthermore, mice lacking the Toll-like receptor (TLR) 4 for LPS were resistant to neurophysiological changes following LPS consumption. These findings demonstrate that ingestion of LPS during a single period specifically and transiently inhibits neural responses to sucrose. We suggest that LPS drinking initiates TLR4-dependent hormonal signals that downregulate sweet taste receptor genes in taste buds. Delayed inhibition of sweet taste signaling may influence food selection and the complex interplay between gastrointestinal bacteria and obesity.