Study of the in vivo role of Mce2R, the transcriptional regulator of mce2 operon in Mycobacterium tuberculosis

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Background: Tuberculosis is one of the leading causes of mortality throughout the world. Mycobacterium tuberculosis, the agent of human tuberculosis, has developed strategies involving proteins and other compounds called virulence factors to subvert human host defences and damage and invade the huma...

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Detalles Bibliográficos
Otros Autores: Forrellad, Marina Andrea, Bianco, María Verónica, Blanco, Federico Carlos, Nuñez, Javier, Klepp, Laura Inés, Vázquez, Cristina Lourdes, Santangelo, María de la Paz, Rocha, Rosana Valeria, Soria, Marcelo Abel, Golby, Paul, Gutierrez, Maximiliano Gabriel, Bigi, Fabiana
Formato: Artículo
Lenguaje:Inglés
Materias:
MCE2R
MYCOBACTERIUM TUBERCULOSIS
PHAGOSOME ARRESTING
BACTERIAL VIRULENCE
HOST RESISTANCE
IN VIVO STUDY
MACROPHAGE
MORTALITY
NONHUMAN
OPERON
PHAGOSOME
REGULON
REVERSE TRANSCRIPTION POLYMERASE CHAIN REACTION
WILD TYPE
MUS
Acceso en línea:http://ri.agro.uba.ar/files/download/articulo/2013forrellad.pdf
LINK AL EDITOR
Aporte de:Registro referencial: Solicitar el recurso aquí
Biblioteca Central (FAUBA) de Universidad de Buenos Aires
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245 1 0 |a Study of the in vivo role of Mce2R, the transcriptional regulator of mce2 operon in Mycobacterium tuberculosis 
520 |a Background: Tuberculosis is one of the leading causes of mortality throughout the world. Mycobacterium tuberculosis, the agent of human tuberculosis, has developed strategies involving proteins and other compounds called virulence factors to subvert human host defences and damage and invade the human host. Among these virulence-related proteins are the Mce proteins, which are encoded in the mce1, mce2, mce3 and mce4 operons of M. tuberculosis. The expression of the mce2 operon is negatively regulated by the Mce2R transcriptional repressor. Here we evaluated the role of Mce2R during the infection of M. tuberculosis in mice and macrophages and defined the genes whose expression is in vitro regulated by this transcriptional repressor. Results: We used a specialized transduction method for generating a mce2R mutant of M. tuberculosis H37Rv. Although we found equivalent replication of the Mtdeltamce2R mutant and the wild type strains in mouse lungs, overexpression of Mce2R in the complemented strain [Mtdeltamce2RComp] significantly impaired its replication. During in vitro infection of macrophages, we observed a significantly increased association of the late endosomal marker LAMP-2 to Mtdeltamce2RComp-containing phagosomes as compared to Mtdeltamce2R and the wild type strains. Whole transcriptional analysis showed that Mce2R regulates mainly the expression of the mce2 operon, in the in vitro conditions studied. Conclusions: The findings of the current study indicate that Mce2R weakly represses the in vivo expression of the mce2 operon in the studied conditions and argue for a role of the proteins encoded in Mce2R regulon in the arrest of phagosome maturation induced by M. tuberculosis. 
653 0 |a MCE2R 
653 0 |a MYCOBACTERIUM TUBERCULOSIS 
653 0 |a PHAGOSOME ARRESTING 
653 0 |a BACTERIAL VIRULENCE 
653 0 |a HOST RESISTANCE 
653 0 |a IN VIVO STUDY 
653 0 |a MACROPHAGE 
653 0 |a MORTALITY 
653 0 |a MYCOBACTERIUM TUBERCULOSIS 
653 0 |a NONHUMAN 
653 0 |a OPERON 
653 0 |a PHAGOSOME 
653 0 |a REGULON 
653 0 |a REVERSE TRANSCRIPTION POLYMERASE CHAIN REACTION 
653 0 |a WILD TYPE 
653 0 |a MUS 
700 1 |a Forrellad, Marina Andrea  |9 67949 
700 1 |a Bianco, María Verónica  |9 48056 
700 1 |9 70699  |a Blanco, Federico Carlos 
700 1 |a Nuñez, Javier  |9 72504 
700 1 |a Klepp, Laura Inés  |9 68513 
700 1 |a Vázquez, Cristina Lourdes  |9 67948 
700 1 |9 72505  |a Santangelo, María de la Paz 
700 1 |a Rocha, Rosana Valeria  |9 67950 
700 1 |9 49057  |a Soria, Marcelo Abel 
700 1 |a Golby, Paul  |9 67951 
700 1 |a Gutierrez, Maximiliano Gabriel  |9 72506 
700 1 |9 48059  |a Bigi, Fabiana 
773 |t BMC Microbiology  |g vol.13, no.1 (2013), p.2-9  
856 |u http://ri.agro.uba.ar/files/download/articulo/2013forrellad.pdf  |i En internet  |q application/pdf  |f 2013forrellad  |x MIGRADOS2018 
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900 |a ^aBlanco^bF. C. 
900 |a ^aNuñez^bJ. 
900 |a ^aKlepp^bL. I. 
900 |a ^aVazquez^bC. L. 
900 |a ^aSantangelo^bM. D. L. P. 
900 |a ^aRocha^bR. V. 
900 |a ^aSoria^bM. A. 
900 |a ^aGolby^bP. 
900 |a ^aGutierrez^bM. G. 
900 |a ^aBigi^bF. 
900 |a ^aForrellad, M.A.^tInstituto de Biotecnología, CICVyA-INTA, N. Repetto and De los Reseros, Hurlingham 1686, Argentina 
900 |a ^aBianco, M.V.^tInstituto de Biotecnología, CICVyA-INTA, N Repetto and De los Reseros, Hurlingham 1686, Argentina 
900 |a ^aBlanco, F.C.^tInstituto de Biotecnología, CICVyA-INTA, N.Repetto and De los Reseros, Hurlingham 1686, Argentina 
900 |a ^aNuñez, J.^tAnimal Health Veterinary Laboratories Agency (Weybridge), New Haw, Addlestone, Surrey KT15 3NB, United Kingdom 
900 |a ^aKlepp, L.I.^tInstituto de Biotecnología, CICVyA-INTA, N. Repetto and De los Reseros, Hurlingham 1686, Argentina 
900 |a ^aVazquez, C.L.^tResearch Group Phagosome Biology, Helmholtz Centre for Infection Research, Inhoffenstrasse 7, Braunschweig 38124, Germany 
900 |a ^aSantangelo, M.D.L.P.^tInstituto de Biotecnología, CICVyA-INTA, N. Repetto and De los Reseros, Hurlingham 1686, Argentina 
900 |a ^aRocha, R.V.^tInstituto de Biotecnología, CICVyA-INTA, N. Repetto and De los Reseros, Hurlingham 1686, Argentina 
900 |a ^aSoria, M.^tMicrobiología Agrícola Facultad de Agronomía, Universidad de Buenos Aires, Avenue San Martín 4453, Buenos Aires 1417, Argentina 
900 |a ^aGolby, P.^tAnimal Health Veterinary Laboratories Agency (Weybridge), New Haw, Addlestone, Surrey KT15 3NB, United Kingdom 
900 |a ^aGutierrez, M.G.^tResearch Group Phagosome Biology, Helmholtz Centre for Infection Research, Inhoffenstrasse 7, Braunschweig 38124, Germany 
900 |a ^aGutierrez, M.G.^tDivision of Mycobacterial Research, MRC National Institute for Medical Research, The Ridgeway, Mill Hill, London NW7 1AA, United Kingdom 
900 |a ^aBigi, F.^tInstituto de Biotecnología, CICVyA-INTA, N. Repetto and De los Reseros, Hurlingham 1686, Argentina 
900 |a ^tBMC Microbiology^cBMC Microbiol. 
900 |a en 
900 |a 13:200 
900 |a ^i 
900 |a Vol. 13, no. 1 
900 |a MCE2R 
900 |a MYCOBACTERIUM TUBERCULOSIS 
900 |a PHAGOSOME ARRESTING 
900 |a BACTERIAL VIRULENCE 
900 |a HOST RESISTANCE 
900 |a IN VIVO STUDY 
900 |a MACROPHAGE 
900 |a MORTALITY 
900 |a MYCOBACTERIUM TUBERCULOSIS 
900 |a NONHUMAN 
900 |a OPERON 
900 |a PHAGOSOME 
900 |a REGULON 
900 |a REVERSE TRANSCRIPTION POLYMERASE CHAIN REACTION 
900 |a WILD TYPE 
900 |a MUS 
900 |a Background: Tuberculosis is one of the leading causes of mortality throughout the world. Mycobacterium tuberculosis, the agent of human tuberculosis, has developed strategies involving proteins and other compounds called virulence factors to subvert human host defences and damage and invade the human host. Among these virulence-related proteins are the Mce proteins, which are encoded in the mce1, mce2, mce3 and mce4 operons of M. tuberculosis. The expression of the mce2 operon is negatively regulated by the Mce2R transcriptional repressor. Here we evaluated the role of Mce2R during the infection of M. tuberculosis in mice and macrophages and defined the genes whose expression is in vitro regulated by this transcriptional repressor. Results: We used a specialized transduction method for generating a mce2R mutant of M. tuberculosis H37Rv. Although we found equivalent replication of the Mtdeltamce2R mutant and the wild type strains in mouse lungs, overexpression of Mce2R in the complemented strain [Mtdeltamce2RComp] significantly impaired its replication. During in vitro infection of macrophages, we observed a significantly increased association of the late endosomal marker LAMP-2 to Mtdeltamce2RComp-containing phagosomes as compared to Mtdeltamce2R and the wild type strains. Whole transcriptional analysis showed that Mce2R regulates mainly the expression of the mce2 operon, in the in vitro conditions studied. Conclusions: The findings of the current study indicate that Mce2R weakly represses the in vivo expression of the mce2 operon in the studied conditions and argue for a role of the proteins encoded in Mce2R regulon in the arrest of phagosome maturation induced by M. tuberculosis. 
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