Protection from pyelonephritis during glucosuria

糖尿期间预防肾盂肾炎

• 批准号: 509466277
• 负责人: Professorin Dr. Sibylle von Vietinghoff
• 金额: --
• 依托单位: Medizinische Klinik und Poliklinik I - Allgemeine Innere Medizin
• 依托单位国家: 德国
• 项目类别: Research Units
• 资助国家: 德国
• 项目状态: 未结题
• 来源: https://gepris.dfg.de/gepris/projekt/509466277?language=en
• 关键词: Protection; pyelonephritis; during; glucosuria

Glucose promotes bacterial growth. Under normal conditions, it is effectively removed from the primary urine by active transport, chiefly by the SGLT2 transporter. Clinical indications for SGLT2 inhibitor use have markedly expanded in the recent past. Beyond diabetes, they now are recommended for heart failure and chronic kidney disease. However, overall upper urinary tract infection rates were unaltered in the sizeable number of randomized controlled trials. The aim of this project is to define antibacterial mechanisms in renal glucosuria. The planned experiments will address tubular epithelial and innate immune defense mechanisms and regulation of bacterial virulence factors by glucose and pharmacologic SGTL2 inhibitors in human cell and bacterial culture and in a murine pyelonephritis model in vivo. Human renal biopsy and urine analyses will serve to validate individual factors. Resulting mechanisms could provide new angles to protect the urinary tract against bacterial infection.

葡萄糖促进细菌生长。在正常情况下，它通过主动转运（主要是SGLT 2转运蛋白）从原发性尿液中有效清除。近年来，SGLT 2抑制剂使用的临床适应症显着扩大。除了糖尿病，它们现在被推荐用于心力衰竭和慢性肾脏疾病。然而，在相当数量的随机对照试验中，总体上尿路感染率没有改变。本项目的目的是确定肾性糖尿的抗菌机制。计划的实验将解决肾小管上皮和先天性免疫防御机制，以及葡萄糖和药理学SGTL2抑制剂在人细胞和细菌培养物中以及在体内小鼠肾盂肾炎模型中对细菌毒力因子的调节。人肾活检和尿液分析将用于验证个体因素。由此产生的机制可以提供新的角度来保护尿路免受细菌感染。