000165910 001__ 165910
000165910 005__ 20260116002211.0
000165910 0247_ $$2doi$$a10.1371/journal.pone.0045213
000165910 0248_ $$2sideral$$a78879
000165910 037__ $$aART-2012-78879
000165910 041__ $$aeng
000165910 100__ $$aAporta, A.$$uUniversidad de Zaragoza
000165910 245__ $$aAttenuated Mycobacterium tuberculosis SO2 Vaccine Candidate Is Unable to Induce Cell Death
000165910 260__ $$c2012
000165910 5060_ $$aAccess copy available to the general public$$fUnrestricted
000165910 5203_ $$at has been proposed that Mycobacterium tuberculosis virulent strains inhibit apoptosis and trigger cell death by necrosis of host macrophages to evade innate immunity, while non-virulent strains induce typical apoptosis activating a protective host response. As part of the characterization of a novel tuberculosis vaccine candidate, the M. tuberculosis phoP mutant SO2, we sought to evaluate its potential to induce host cell death. The parental M. tuberculosis MT103 strain and the current vaccine against tuberculosis Bacillus Calmette-Guérin (BCG) were used as comparators in mouse models in vitro and in vivo. Our data reveal that attenuated SO2 was unable to induce apoptotic events neither in mouse macrophages in vitro nor during lung infection in vivo. In contrast, virulent MT103 triggers typical apoptotic events with phosphatidylserine exposure, caspase-3 activation and nuclear condensation and fragmentation. BCG strain behaved like SO2 and did not induce apoptosis. A clonogenic survival assay confirmed that viability of BCG- or SO2-infected macrophages was unaffected. Our results discard apoptosis as the protective mechanism induced by SO2 vaccine and provide evidence for positive correlation between classical apoptosis induction and virulent strains, suggesting apoptosis as a possible virulence determinant during M. tuberculosis infection.
000165910 540__ $$9info:eu-repo/semantics/openAccess$$aby$$uhttps://creativecommons.org/licenses/by/4.0/deed.es
000165910 590__ $$a3.73$$b2012
000165910 591__ $$aMULTIDISCIPLINARY SCIENCES$$b7 / 57 = 0.123$$c2012$$dQ1$$eT1
000165910 655_4 $$ainfo:eu-repo/semantics/article$$vinfo:eu-repo/semantics/publishedVersion
000165910 700__ $$0(orcid)0000-0002-3377-4171$$aArbues, A.
000165910 700__ $$0(orcid)0000-0001-7897-9173$$aAguilo, J. I.$$uUniversidad de Zaragoza
000165910 700__ $$0(orcid)0000-0002-2787-9671$$aMonzon, M.$$uUniversidad de Zaragoza
000165910 700__ $$0(orcid)0000-0002-7173-7216$$aBadiola, J. J.$$uUniversidad de Zaragoza
000165910 700__ $$ade Martino, A.
000165910 700__ $$aFerrer, N.
000165910 700__ $$aMarinova, D.
000165910 700__ $$0(orcid)0000-0002-5175-8394$$aAnel, A.$$uUniversidad de Zaragoza
000165910 700__ $$0(orcid)0000-0003-2993-5478$$aMartin, C.$$uUniversidad de Zaragoza
000165910 700__ $$0(orcid)0000-0003-0154-0730$$aPardo, J.$$uUniversidad de Zaragoza
000165910 7102_ $$11008$$2630$$aUniversidad de Zaragoza$$bDpto. Microb.Med.Pr.,Sal.Públ.$$cÁrea Microbiología
000165910 7102_ $$11009$$2773$$aUniversidad de Zaragoza$$bDpto. Patología Animal$$cÁrea Sanidad Animal
000165910 7102_ $$11008$$2566$$aUniversidad de Zaragoza$$bDpto. Microb.Med.Pr.,Sal.Públ.$$cÁrea Inmunología
000165910 7102_ $$11002$$2X$$aUniversidad de Zaragoza$$bDpto. Bioq.Biolog.Mol. Celular$$cProy. investigación DEA
000165910 7102_ $$11002$$2060$$aUniversidad de Zaragoza$$bDpto. Bioq.Biolog.Mol. Celular$$cÁrea Bioquímica y Biolog.Mole.
000165910 773__ $$g7, 9 (2012), e45213 [11 pp.]$$pPLoS One$$tPLoS ONE$$x1932-6203
000165910 8564_ $$s4624017$$uhttps://zaguan.unizar.es/record/165910/files/texto_completo.pdf$$yVersión publicada
000165910 8564_ $$s3359602$$uhttps://zaguan.unizar.es/record/165910/files/texto_completo.jpg?subformat=icon$$xicon$$yVersión publicada
000165910 909CO $$ooai:zaguan.unizar.es:165910$$particulos$$pdriver
000165910 951__ $$a2026-01-15-21:56:24
000165910 980__ $$aARTICLE