Elevated cAMP levels reverse Brucella melitensis-induced lipid peroxidation and stimulate IL-10 transcription in rats

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dc.contributor.authorErdogan, S.
dc.contributor.authorCelik, S.
dc.contributor.authorAslantas, O.
dc.contributor.authorKontas, T.
dc.contributor.authorOcak, S.
dc.date.accessioned2024-09-18T20:06:15Z
dc.date.available2024-09-18T20:06:15Z
dc.date.issued2007
dc.departmentHatay Mustafa Kemal Üniversitesien_US
dc.description.abstractBrucella species are able to survive and replicate within the phagocytic vacuole of macrophages that induce chronic infection in humans and domestic animals. The activation of oxidative bactericidal activity is one of the defense systems which protect the host from the toxic effects of pathogens. The aim of this study was to evaluate lipid peroxidation, NO production, antioxidative system and inflammation during a period of brucella infection in a rat model; in addition to investigate the role of elevated intracellular cyclic AMP on Brucella-induced events. Brucella significantly induced lipid peroxidation in plasma, liver and spleen by 3-5-fold at 7 days postinfection. NO concentration was significantly elevated in the liver and spleen while unchanged in plasma. Cyclic AMP elevating agent, rolipram, administration (1 mg/kg/day i.p., 3 days) gradually suppressed lipid peroxidation and NO formation to the basal level in plasma and spleen whilst only a slight decrease was observed in liver. Brucella considerably decreased SOD activity in the liver and spleen, with rolipram restoring the enzyme activity in liver and activity in spleen being unchanged. Reverse transcriptase PCR analyses showed that Brucella melitensis does not alter TNF-alpha and IFN-gamma transcriptions in liver and spleen. The pathogen did not consistently induce nitric oxide synthase mRNA transcriptions in animals; even in those housed in the same group. IL-10 transcription was induced by rolipram in spleen but not in liver. Our results suggest that activation of the cAMP/PKA pathway suppressed lipid peroxidation and the elevated NO concentrations caused by B. melitensis, Moreover, rolipram induced anti-inflammatory cytokine IL-10 transcription and SOD activity, albeit in a tissue dependent manner. (c) 2006 Elsevier Ltd. All rights reserved.en_US
dc.identifier.doi10.1016/j.rvsc.2006.07.008
dc.identifier.endpage186en_US
dc.identifier.issn0034-5288
dc.identifier.issn1532-2661
dc.identifier.issue2en_US
dc.identifier.pmid17014875en_US
dc.identifier.scopus2-s2.0-33846787121en_US
dc.identifier.scopusqualityQ1en_US
dc.identifier.startpage181en_US
dc.identifier.urihttps://doi.org/10.1016/j.rvsc.2006.07.008
dc.identifier.urihttps://hdl.handle.net/20.500.12483/8413
dc.identifier.volume82en_US
dc.identifier.wosWOS:000244921000007en_US
dc.identifier.wosqualityQ1en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherElsevier Sci Ltden_US
dc.relation.ispartofResearch in Veterinary Scienceen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectBrucella melitensisen_US
dc.subjectcAMPen_US
dc.subjectcytokineen_US
dc.subjectMDAen_US
dc.subjectoxidative stressen_US
dc.subjectrolipramen_US
dc.subjectlipid peroxidationen_US
dc.titleElevated cAMP levels reverse Brucella melitensis-induced lipid peroxidation and stimulate IL-10 transcription in ratsen_US
dc.typeArticleen_US

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