Escherichia coli-induced inducible nitric oxide synthase and cyclooxygenase expression in the mouse bladder and kidney
Forskningsoutput: Tidskriftsbidrag › Artikel i vetenskaplig tidskrift
BACKGROUND: The host response to urinary tract infection includes the production of different inflammatory mediators. We investigated the cellular localization and time course of inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX-2) expression in the mouse bladder and kidney after bacterial infection. METHODS: Experimental urinary tract infection in mice was established by intravesical inoculation of a clinical uropathogen Escherichia coli (E. coli) AD 110. Urine was collected at 6-, 12-, 24-, and 72-hours postinstillation, and the nitrite concentration was determined. The induction of iNOS and COX-2 was studied by immunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: Nitrite levels in the urine had increased threefold at 6 and 12 hours postbacterial instillation. Bladders from mice instilled with AD 110, but not with phosphate-buffered saline, showed a large number of iNOS-- and COX-2--expressing inflammatory cells. The inflammatory cell activation peaked at 6 and 12 hours postinstillation and had vanished by 72 hours. iNOS expression was detected in some urothelial cells after 24 and 72 hours, but COX-2 expression was not detected. In the kidney, infection activated an iNOS and COX-2 response, as shown by immunoreactivity in inflammatory cells at all time points. A strong epithelial iNOS response was observed in the renal pelvis at 12, 24, and 72 hours postinstillation, but COX-2 was not detected. Enhanced tissue expression of iNOS and COX-2 after bacterial instillation was also demonstrated by RT-PCR. CONCLUSIONS: E. coli AD 110 induced expression of iNOS and COX-2 in the urinary tract. Inflammatory cells expressed both iNOS-and COX-2, but epithelial cells expressed only iNOS and with a later onset than in the inflammatory cells. This suggests that the epithelial iNOS response is not caused by direct bacterial activation, but more likely is by mediators involved in the inflammatory response.
|Enheter & grupper|
Ämnesklassifikation (UKÄ) – OBLIGATORISK
|Status||Published - 2001|
|Peer review utförd||Ja|