Cisplatin reduces Brucella melitensis-infected cell number by inducing apoptosis, oxidant and pro-inflammatory cytokine production

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dc.contributor.authorErdogan, Suat
dc.contributor.authorTosyali, Eda
dc.contributor.authorDuzguner, Vesile
dc.contributor.authorKucukgul, Altug
dc.contributor.authorAslantas, Ozkan
dc.contributor.authorCelik, Sefa
dc.date.accessioned2024-09-18T20:06:15Z
dc.date.available2024-09-18T20:06:15Z
dc.date.issued2010
dc.departmentHatay Mustafa Kemal Üniversitesien_US
dc.description.abstractBrucella species are able to survive and replicate within the phagocytic cells and cause chronic infections in domestic animals and humans. Modulation of programmed cell death by Brucella spp. may be one of the reasons of the chronicity of the infection. In this study, whether cisplatin treatment, an apoptotic anticancer agent, would enhance the host resistance against Brucella melitensis-infected human macrophage-like cells was investigated. The infection neither induced inflammation nor oxidative stress. But, Brucella caused a decrease in infected macrophage viability of 36% at 48 h postinfection (p.i.) as compared with uninfected cells. Treatment of infected macrophages with 20 mu M cisplatin for 48 h caused a large increase in nitric oxide (NO) levels in a time-dependent manner via induction of iNOS transcription. Cisplatin also enhanced glutathione peroxidase, myeloperoxidase and xanthine oxidase activities, providing evidence of generation of reactive free radicals. N-acetylcysteine was able to decrease cisplatin-induced NO, and prevented the agent-induced apoptosis, similar to effects found in L-NAME (N(G)-nitro-L-arginine methyl ester) treatment. Cisplatin stimulated inflammation through the induction of TNF-alpha and IL-12 secretion, and down-regulated Brucella-stimulated IL-10 transcription. The number of infected cells and their viability were decreased by 80% at 48 h p.i. by cisplatin in comparison with infected cells. Similar to this result, cisplatin treatment resulted in reduced intracellular CFU of B. melitensis being reduced by 80% at 48 h p.i. These findings demonstrate that pharmacological agents such as cisplatin may be considered to influence immune responses and apoptosis to help decrease Brucella-infected cell number. (C) 2009 Elsevier Ltd. All rights reserved.en_US
dc.description.sponsorshipScientific and Technological Research Council of Turkey [TOVAG-105O407]; Scientific Research Projects Commission of MKU [07G0101]; Turkish Academy of Sciences (TUBA) [GEBIP-2005]en_US
dc.description.sponsorshipThis work was supported by a grant from the Scientific and Technological Research Council of Turkey (TOVAG-105O407) and in part from the Scientific Research Projects Commission of MKU (07G0101) and Turkish Academy of Sciences (TUBA, GEBIP-2005). We thank Prof. Dr. Miles D. Houslay (Glasgow University, Scotland/UK) for providing U937 cells. Authors wish to thank Dr. Sandra Spence for her helpful reading of the manuscript.en_US
dc.identifier.doi10.1016/j.rvsc.2009.09.002
dc.identifier.endpage226en_US
dc.identifier.issn0034-5288
dc.identifier.issn1532-2661
dc.identifier.issue2en_US
dc.identifier.pmid19818462en_US
dc.identifier.scopus2-s2.0-76849095168en_US
dc.identifier.scopusqualityQ1en_US
dc.identifier.startpage218en_US
dc.identifier.urihttps://doi.org/10.1016/j.rvsc.2009.09.002
dc.identifier.urihttps://hdl.handle.net/20.500.12483/8414
dc.identifier.volume88en_US
dc.identifier.wosWOS:000275970100006en_US
dc.identifier.wosqualityQ2en_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.subjectCisplatinen_US
dc.subjectApoptosisen_US
dc.subjectNitric oxideen_US
dc.subjectInflammationen_US
dc.titleCisplatin reduces Brucella melitensis-infected cell number by inducing apoptosis, oxidant and pro-inflammatory cytokine productionen_US
dc.typeArticleen_US

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