In the present study, we investigated whether cellular damage, as demonstrated by lactate dehydrogenase<br/>(LDH) release in the human fallopian tube (FT) infected by Neisseria gonorrhoeae (Ngo), correlated with<br/>high levels of nitric oxide synthase (NOS) mRNA and enzyme activity. Infection with Ngo induced a<br/>significant increase (~35-fold) in mRNA transcripts of the inducible isoform of NOS. <br/><br/>Paradoxically, a reduction in NOS enzyme activity was observed in infected cultures, suggesting that gonococcal infection possibly influences translation of iNOS mRNA to the enzyme. In addition, treatment with the NOS inhibitor<br/>TRIM did not prevent gonococcal-induced cellular damage. In contrast, the addition of the inhibitor L-NAME induced a 40% reduction in LDH release, which correlated with a ~50% reduction in gonococcal numbers.<br/><br/>Moreover, treatment of normal FT explants with an exogenous NO donor, SNAP, did not induce significant<br/>cellular damage. Taken together, our data suggest that NO does not contribute to cellular damage during<br/>infection of the human FT with Neisseria gonorrhoeae
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