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Am J Physiol Renal Physiol (September 3, 2002). doi:10.1152/ajprenal.00101.2002
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Articles in PresS, published online ahead of print September 3, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00101.2002
Submitted on March 15, 2002
Accepted on September 1, 2002

Urinary tract infection in iNOS deficient mice with focus on bacterial sensitivity to nitric oxide

Mirjana Poljakovic1* and Katarina Persson2

1 Department of Clinical Pharmacology, Lund University Hospital, Lund, Sweden
2 Department of Clinical Pharmacology, Lund University Hospital, Lund, Sweden; Department of Chemistry and Biomedical Sciences, University of Kalmar, Kalmar, Sweden

* To whom correspondence should be addressed. E-mail: mirjana.poljakovic{at}klinfarm.lu.se.

iNOS deficient mice were used to examine the role of iNOS in E. 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 SIN-1, while the avirulent E. coli HB101 was sensitive to both NO and SIN-1. 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, nNOS and eNOS 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 the bacterial virulence. Furthermore, myeloperoxidase and nNOS/eNOS may contribute to nitrotyrosine formation in the absence of iNOS.




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