Uropathogenic Escherichia coli-Induced Inflammation Alters Mouse Urinary Bladder Contraction via an Interleukin-6-Activated Inducible Nitric Oxide Synthase-Related Pathway

摘要: Escherichia coli is the most common cause of urinary tract infection. Elevated blood and urine interleukin-6 (IL-6) levels have been shown in inflammatory diseases. The role IL-6 mediating urodynamic dysfunction response to E. coli-induced infection has not yet fully elucidated. In this study, we investigated nitric oxide (NO)-triggered alteration contractile responses bladder under an condition. electrical field stimulation (EFS)-evoked contractions isolated detrusor strips, immunoblotting for detecting protein expression bladders was measured short term (1 h) or long (6 24 after intraperitoneal injection endotoxin (lipopolysaccharide [LPS]) intravesical instillation human pyelonephritogenic coli-J96 (O4:K6) strain LPS into mice. NO productions were increased mice 1 h treatment. Inducible synthase (iNOS) kinase C (PKC) activation EFS-evoked at 6 treatment, which could be reversed by anti-IL-6 antibody iNOS inhibitor aminoguanidine. At administration, generation, endothelial NOS expression, effectively increased, whereas reverse these LPS-induced responses. These results indicate that may play important iNOS/NO-triggered PKC-activated during inflammation.