| First Author | Poljakovic M | Year | 2003 |
| Journal | Am J Physiol Renal Physiol | Volume | 284 |
| Issue | 1 | Pages | F22-31 |
| PubMed ID | 12494944 | Mgi Jnum | J:127929 |
| Mgi Id | MGI:3765225 | Doi | 10.1152/ajprenal.00101.2002 |
| Citation | Poljakovic M, et al. (2003) Urinary tract infection in iNOS-deficient mice with focus on bacterial sensitivity to nitric oxide. Am J Physiol Renal Physiol 284(1):F22-31 |
| abstractText | Inducible nitric oxide synthase (iNOS)-deficient mice were used to examine the role of iNOS in Escherichia coli-induced urinary tract infection (UTI). The toxicity of nitric oxide (NO)/peroxynitrite to bacteria and host was also investigated. The nitrite levels in urine of iNOS+/+ but not iNOS/ mice increased after infection. No differences in bacterial clearance or persistence were noted between the genotypes. In vitro, the uropathogenic E. coli 1177 was sensitive to 3-morpholinosydnonimine, whereas the avirulent E. coli HB101 was sensitive to both NO and 3-morpholinosydnonimine. E. coli HB101 was statistically (P < 0.05) more sensitive to peroxynitrite than E. coli 1177. Nitrotyrosine immunoreactivity was observed in infected bladders of both genotypes and in infected kidneys of iNOS+/+ mice. Myeloperoxidase, neuronal (n)NOS, and endothelial (e)NOS immunoreactivity was observed in inflammatory cells of both genotypes. Our results indicate that iNOS/ and iNOS+/+ mice are equally susceptible to E. coli-induced UTI and that the toxicity of NO to E. coli depends on bacterial virulence. Furthermore, myeloperoxidase and nNOS/eNOS may contribute to nitrotyrosine formation in the absence of iNOS. |
