Nitric oxide is not involved in Neisseria gonorrhoeae-induced cellular damage of human fallopian tubes in vitro
Garcia, Katherine, Rubilar, Paulina S., Vargas, Macarena F., Cardenas, Hugo, Rios, Miguel A., Orihuela, Pedro A., Vargas, Renato H., Fuhrer, Juan, Heckels, John E., Christodoulides, Myron and Velasquez, Luis A. (2010) Nitric oxide is not involved in Neisseria gonorrhoeae-induced cellular damage of human fallopian tubes in vitro. Biological Research, 43, 39-50. (doi:10.4067/S0716-97602010000100006).
In the present study, we investigated whether cellular damage, as demonstrated by lactate dehydrogenase
(LDH) release in the human fallopian tube (FT) infected by Neisseria gonorrhoeae (Ngo), correlated with
high levels of nitric oxide synthase (NOS) mRNA and enzyme activity. Infection with Ngo induced a
significant increase (~35-fold) in mRNA transcripts of the inducible isoform of NOS.
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
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.
Moreover, treatment of normal FT explants with an exogenous NO donor, SNAP, did not induce significant
cellular damage. Taken together, our data suggest that NO does not contribute to cellular damage during
infection of the human FT with Neisseria gonorrhoeae.
|Digital Object Identifier (DOI):||doi:10.4067/S0716-97602010000100006|
|Keywords:||cellular damage, fallopian tubes, neisseria gonorrhoeae, nitric oxide|
|Subjects:||R Medicine > RG Gynecology and obstetrics
R Medicine > RC Internal medicine
|Divisions:||University Structure - Pre August 2011 > School of Medicine > Infection, Inflammation and Repair
|Date Deposited:||14 Jul 2010 12:58|
|Last Modified:||27 Mar 2014 19:16|
|RDF:||RDF+N-Triples, RDF+N3, RDF+XML, Browse.|
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