Condron Claire, Casey Rowan G, Kehoe Siobhan, Toomey Deirdre, Creagh Tom, Bouchier-Hayes David J
Department of Surgery, Royal College of Surgeons in Ireland, Beaumont Hospital, Dublin, Ireland.
Urol Res. 2010 Aug;38(4):215-22. doi: 10.1007/s00240-009-0235-z. Epub 2009 Nov 26.
Eradication of a urinary tract infection (UTI) appears to be related to a number of innate host defence mechanisms and their interactions with invading bacteria. Recurrent UTIs (rUTIs) pose a difficult problem in that these bacteria use both host and bacterial factors to evade elimination. Neutrophil bactericidal function is depressed, both systemically and in urine, in patients with a history of recurrent UTI. Taurine is a semi-essential amino acid and is successful in preserving neutrophil bactericidal function in urine. Taurine may preserve neutrophil function at the urothelium and thus aid UTI resolution. Adult female (6 weeks old) C57Bl/6 mice were randomised into three groups: a saline gavage only control group, a saline gavage + E. coli group, and a taurine gavage + E. coli group [21 g/70 kg taurine in 0.9% normal saline (N/S) for 5 days]. Whilst taurine gavage pre-treatment resulted in increased serum neutrophils respiratory burst activity, at the urothelial-endothelial interface it caused higher colony forming units in the urine and a higher incidence of E. coli invasion in the bladder wall with no evidence of increased bladder wall neutrophils infiltration on MPO assay of histological assessment. Histologically there was also evidence of reduced bladder inflammation and urothelial cell apoptosis. In conclusion, taurine effectively increases neutrophils activity but given its anti-inflammatory properties, at the expense of decreased urothelial-endothelial activation thus preventing clearance of active E. coli infection in the bladder. Despite the negative results, this study demonstrates the importance of modulating interactions at the urothelial interface.
根除尿路感染(UTI)似乎与多种先天性宿主防御机制及其与入侵细菌的相互作用有关。复发性尿路感染(rUTIs)带来了一个难题,即这些细菌利用宿主和细菌因素来逃避清除。有复发性尿路感染病史的患者,其全身和尿液中的中性粒细胞杀菌功能均受到抑制。牛磺酸是一种半必需氨基酸,可成功维持尿液中的中性粒细胞杀菌功能。牛磺酸可能在尿路上皮维持中性粒细胞功能,从而有助于尿路感染的消退。将成年雌性(6周龄)C57Bl/6小鼠随机分为三组:仅生理盐水灌胃对照组、生理盐水灌胃+大肠杆菌组和牛磺酸灌胃+大肠杆菌组[21 g/70 kg牛磺酸溶于0.9%生理盐水(N/S),持续5天]。虽然牛磺酸灌胃预处理导致血清中性粒细胞呼吸爆发活性增加,但在尿路上皮-内皮界面,它导致尿液中菌落形成单位增加,膀胱壁大肠杆菌入侵发生率更高,在组织学评估的MPO测定中没有膀胱壁中性粒细胞浸润增加的证据。组织学上也有膀胱炎症减轻和尿路上皮细胞凋亡减少的证据。总之,牛磺酸有效地增加了中性粒细胞活性,但鉴于其抗炎特性,代价是尿路上皮-内皮激活减少,从而阻止了膀胱中活性大肠杆菌感染的清除。尽管结果为阴性,但本研究证明了调节尿路上皮界面相互作用的重要性。