Defects in the peripheral taste structure and function in the MRL/lpr mouse model of autoimmune disease.
Defects in the peripheral taste structure and function in the MRL/lpr mouse model of autoimmune disease.
复制标题
自身免疫性疾病的MRL/LPR小鼠模型中的外周味道结构和功能的缺陷。
DOI：
10.1371/journal.pone.0035588
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发表时间：
2012
期刊：
影响因子：
3.7
通讯作者：
Wang H
中科院分区：
文献类型：
--
作者：
Kim A;Feng P;Ohkuri T;Sauers D;Cohn ZJ;Chai J;Nelson T;Bachmanov AA;Huang L;Wang H
虽然我们对味觉接受和信号传导的分子和细胞方面的理解不断提高，但导致味觉功能障碍的这些过程中的畸变仍然在很大程度上未被探索。味觉缺失可以在多种疾病中发展，包括感染和自身免疫性疾病。在这项研究中，我们使用自身免疫性疾病的小鼠模型来研究味觉障碍的潜在机制。MRL/MpJ-Faslpr/J（MRL/lpr）小鼠产生了与人类系统性红斑狼疮和干燥综合征表型相似的系统性自身免疫。我们的研究结果表明，MRL/lpr小鼠的味觉组织表现出炎症特征，包括T淋巴细胞浸润和一些炎性细胞因子水平升高。组织学研究表明，MRL/lpr小鼠的味蕾比野生型同类对照（MRL/+/+）小鼠的味蕾要小。5-溴-2 ′-脱氧尿苷（BrdU）脉冲追踪实验表明，进入MRL/lpr小鼠味蕾的BrdU标记细胞较少，提示味觉细胞更新受到抑制。实时RT-PCR分析显示，MRL/lpr小鼠中几种II型味觉细胞标志物的mRNA水平较低。免疫组织化学分析证实MRL/lpr小鼠味蕾中的味蛋白阳性味觉受体细胞的数量显著减少。此外，与对照相比，MRL/lpr小鼠表现出对苦味化合物奎宁和甜味化合物糖精的味觉神经反应降低，以及对苦味、甜味和鲜味物质的行为反应降低。相比之下，在神经记录和行为实验中，它们对咸和酸化合物的反应与对照小鼠相当。总之，我们的研究结果表明，II型味觉受体细胞，这是必不可少的苦，甜，和鲜味的接收和信号，选择性地影响MRL/lpr小鼠，自身免疫性疾病与慢性炎症模型。
While our understanding of the molecular and cellular aspects of taste reception and signaling continues to improve, the aberrations in these processes that lead to taste dysfunction remain largely unexplored. Abnormalities in taste can develop in a variety of diseases, including infections and autoimmune disorders. In this study, we used a mouse model of autoimmune disease to investigate the underlying mechanisms of taste disorders. MRL/MpJ-Faslpr/J (MRL/lpr) mice develop a systemic autoimmunity with phenotypic similarities to human systemic lupus erythematosus and Sjögren's syndrome. Our results show that the taste tissues of MRL/lpr mice exhibit characteristics of inflammation, including infiltration of T lymphocytes and elevated levels of some inflammatory cytokines. Histological studies reveal that the taste buds of MRL/lpr mice are smaller than those of wild-type congenic control (MRL/+/+) mice. 5-Bromo-2′-deoxyuridine (BrdU) pulse-chase experiments show that fewer BrdU-labeled cells enter the taste buds of MRL/lpr mice, suggesting an inhibition of taste cell renewal. Real-time RT-PCR analyses show that mRNA levels of several type II taste cell markers are lower in MRL/lpr mice. Immunohistochemical analyses confirm a significant reduction in the number of gustducin-positive taste receptor cells in the taste buds of MRL/lpr mice. Furthermore, MRL/lpr mice exhibit reduced gustatory nerve responses to the bitter compound quinine and the sweet compound saccharin and reduced behavioral responses to bitter, sweet, and umami taste substances compared with controls. In contrast, their responses to salty and sour compounds are comparable to those of control mice in both nerve recording and behavioral experiments. Together, our results suggest that type II taste receptor cells, which are essential for bitter, sweet, and umami taste reception and signaling, are selectively affected in MRL/lpr mice, a model for autoimmune disease with chronic inflammation.
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影响因子：
4.2
作者：
Cavallin, MA;McCluskey, LP
通讯作者：
McCluskey, LP
影响因子：
2.9
作者：
Boughter JD Jr;Raghow S;Nelson TM;Munger SD
通讯作者：
Munger SD
味觉的细胞生物学。
影响因子：
7.8
作者：
Chaudhari, Nirupa;Roper, Stephen D.
通讯作者：
Roper, Stephen D.
DOI：
10.1159/000093760
发表时间：
2006-01-01
期刊：
TASTE AND SMELL: AN UPDATE
影响因子：
--
作者：
Breslin, Paul A. S.;Huang, Liquan
通讯作者：
Huang, Liquan
影响因子：
2.5
作者：
Clapp, TR;Yang, RB;Kinnamon, JC
通讯作者：
Kinnamon, JC