Departments of Microbiology, University of Alabama at Birmingham, Birmingham, AL, USA.
J Infect Dis. 2010 Mar 15;201(6):866-70. doi: 10.1086/650696.
Group B Streptococcus (GBS) causes urinary tract infections, but the pathogenic mechanisms underlying GBS urinary tract infections are unknown. We investigated whether uropathogenic GBS can bind to bladder uroepithelium to initiate urinary tract infection. Uropathogenic GBS isolated from a patient with acute cystitis bound to human T24 bladder uroepithelial cells in close association with F-actin in statistically significantly higher numbers compared with nonuropathogenic GBS. In vivo modeling using transurethrally infected mice revealed superior fitness of uropathogenic GBS for bladder colonization and potent uropathogenic GBS-specific up-regulation of interleukin 1alpha during infection. Thus, binding of uropathogenic GBS to uroepithelium and vigorous induction of interleukin 1alpha represents the initial stages of GBS urinary tract infection.
B 群链球菌（GBS）可引起尿路感染，但 GBS 尿路感染的发病机制尚不清楚。我们研究了产尿道病原体的 GBS 是否可以与膀胱尿路上皮结合，从而引发尿路感染。从一名急性膀胱炎患者中分离出的产尿道病原体 GBS 与人类 T24 膀胱尿路上皮细胞的结合数量明显高于非产尿道病原体 GBS，而且与 F-肌动蛋白紧密相关。通过经尿道感染的小鼠进行体内建模，揭示了产尿道病原体 GBS 对膀胱定植的更强适应性，以及在感染过程中强烈诱导 GBS 特异性白细胞介素 1α 的表达。因此，产尿道病原体 GBS 与尿路上皮的结合以及白细胞介素 1α 的大量诱导代表了 GBS 尿路感染的初始阶段。
