Effect of T1R3 Taste Receptor Gene Deletion on Dextran Sulfate Sodium-Induced Colitis in Mice
Effect of T1R3 Taste Receptor Gene Deletion on Dextran Sulfate Sodium-Induced Colitis in Mice
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DOI：
10.3177/jnsv.68.204
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发表时间：
2022-01-01
影响因子：
1.6
通讯作者：
Takahashi, Akira
中科院分区：
文献类型：
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作者：
Kondo, Tsubasa;Uebanso, Takashi;Takahashi, Akira
味觉受体1型成员3（T1 R3）识别鲜味或甜味，并分别在小肠和肌肉细胞中促进2型免疫和自噬。由于1型和2型免疫失衡和自噬影响肠道疾病（IBD），我们假设T1 R3在结肠炎的发生和进展中具有潜在的作用。在本研究中，我们研究了T1 R3基因缺失是否会影响DSS诱导的小鼠结肠炎的加重。我们发现，与接受DSS治疗的WT小鼠相比，T1 R3-KO小鼠的结肠损伤有所减少，包括炎症和结肠萎缩减少。T1 R3-KO小鼠中紧密连接组分的mRNA表达，特别是claudin 1的mRNA表达显著降低，结肠中的炎症相关基因mRNA表达有降低的趋势。其他参数，如脾淋巴细胞和腹腔巨噬细胞对微生物刺激的反应，肠道微生物群组成和自噬相关蛋白的表达，在WT和KO小鼠之间相似。总之，这些结果表明，T1 R3的缺失在DSS诱导的小鼠急性结肠炎诱导的肠道炎症中具有次要作用。
Taste receptor type 1 member 3 (T1R3) recognize umami or sweet tastes and also contributes type 2 immunity and autophagy in small intestine and muscle cells, respectively. Since imbalance of type 1 and type 2 immunity and autophagy affect intestinal bowel disease (IBD), we hypothesized that T1R3 have a potential role in the incidence and progression of colitis. In the present study, we investigated whether genetic deletion of T1R3 impacted aggravation of DSS-induced colitis in mice. We found that T1R3-KO mice showed reduction in colon damage, including reduced inflammation and colon shrinking relative to those of WT mice following DSS treatment. mRNA expression of tight junction components, particularly claudin1 was significantly lower in T1R3-KO mice with trend to lower inflammation related gene mRNA expression in colon. Other parameters, such as response to microbial stimuli in splenic lymphocytes and peritoneal macrophages, gut microbiota composition, and expression of autophagy-related proteins, were similar between WT and KO mice. Together, these results indicated that deletion of T1R3 has a minor role in intestinal inflammation induced by DSS-induced acute colitis in mice.