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首页> 外文期刊>Cellular Physiology and Biochemistry >SGLT1 Deficiency Turns Listeria Infection into a Lethal Disease in Mice
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SGLT1 Deficiency Turns Listeria Infection into a Lethal Disease in Mice

机译：SGLT1缺乏症将利斯特氏菌感染转化为小鼠致死性疾病

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>Background: Cellular glucose uptake may involve either non-concentrative glucose carriers of the GLUT family or Na+-coupled glucose-carrier SGLT1, which accumulates glucose against glucose gradients and may thus accomplish cellular glucose uptake even at dramatically decreased extracellular glucose concentrations. SGLT1 is not only expressed in epithelia but as well in tumour cells and immune cells. Immune cell functions strongly depend on their metabolism, therefore we hypothesized that deficiency of SGLT1 modulates the defence against bacterial infection. To test this hypothesis, we infected wild type mice and gene targeted mice lacking functional SGLT1 with Listeria monocytogenes. Methods: SGLT1 deficient mice and wild type littermates were infected with 1x104 CFU Listeria monocytogenes intravenously. Bacterial titers were determined by colony forming assay, SGLT1, TNF-?±, IL-6 and IL-12a transcript levels were determined by qRT-PCR, as well as SGLT1 protein abundance and localization by immunohistochemistry. Results: Genetic knockout of SGLT1 (Slc5a1-/- mice) significantly compromised bacterial clearance following Listeria monocytogenes infection with significantly enhanced bacterial load in liver, spleen, kidney and lung, and significantly augmented hepatic expression of TNF-?± and IL-12a. While all wild type mice survived, all SGLT1 deficient mice died from the infection. Conclusions: SGLT1 is required for bacterial clearance and host survival following murine Listeria infection.
机译：> 背景： 细胞摄取葡萄糖可能涉及GLUT家族的非浓缩葡萄糖载体或与Na + 偶联的葡萄糖载体SGLT1 ，它会针对葡萄糖梯度积累葡萄糖，因此即使在细胞外葡萄糖浓度显着降低的情况下也可以完成细胞对葡萄糖的摄取。 SGLT1不仅在上皮细胞中表达，而且在肿瘤细胞和免疫细胞中也表达。免疫细胞功能在很大程度上取决于其新陈代谢，因此我们假设SGLT1的缺乏会调节抵抗细菌感染的防御能力。为了验证这一假设，我们用单核细胞增生李斯特氏菌感染野生型小鼠和缺乏功能性SGLT1的基因靶向小鼠。 方法： SGLT1缺陷小鼠和野生同窝小鼠静脉感染1x10 4 CFU 单核细胞增生李斯特菌。通过集落形成测定法测定细菌滴度，通过qRT-PCR测定SGLT1，TNF-α，IL-6和IL-12a转录水平，以及通过免疫组织化学测定SGLT1蛋白的丰度和定位。 结果： SGLT1（ Slc5a1 -/- 小鼠）的基因敲除严重损害了李斯特菌感染后的细菌清除率单核细胞增生李斯特氏菌感染，可显着增强肝脏，脾脏，肾脏和肺中的细菌负荷，并显着增强肝组织中TNF-α和IL-12a的表达。尽管所有野生型小鼠均存活，但所有SGLT1缺陷型小鼠均因感染而死亡。 结论： 鼠李斯特氏菌感染后细菌清除和宿主存活需要SGLT1。

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