Mycobacterium tuberculosisInduction of Heme Oxygenase-1 Expression Is Dependent on Oxidative Stress and Reflects Treatment Outcomes

Detalhes bibliográficos
Autor(a) principal: Rockwood, Neesha
Data de Publicação: 2017
Outros Autores: Costa, Diego Luis, Amaral, Eduardo Pinheiro, Du Bruyn, Elsa, Kubler, Andre, Gil-Santana, Leonardo, Fukutani, Kiyoshi F, Scanga, Charles A, Flynn, JoAnne L, Jackson, Sharon H, Wilkinson, Katalin A, Bishai, William R, Sher, Alan, Wilkinson, Robert J, Andrade, Bruno de Bezerril
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da FIOCRUZ (ARCA)
Texto Completo: https://www.arca.fiocruz.br/handle/icict/25556
Resumo: Intramural Research Program of the NIAID and by a grant from the National Institutes of Health (NIH) U01AI115940. RW is supported by the Francis Crick Institute which receives its core funding from Câncer Research UK (FC00110218), the UK Medical Research Council
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spelling Rockwood, NeeshaCosta, Diego LuisAmaral, Eduardo PinheiroDu Bruyn, ElsaKubler, AndreGil-Santana, LeonardoFukutani, Kiyoshi FScanga, Charles AFlynn, JoAnne LJackson, Sharon HWilkinson, Katalin ABishai, William RSher, AlanWilkinson, Robert JAndrade, Bruno de Bezerril2018-04-02T14:08:02Z2018-04-02T14:08:02Z2017ROCKWOOD, N. et al. Mycobacterium tuberculosisInduction of Heme Oxygenase-1 Expression Is Dependent on Oxidative Stress and Reflects Treatment Outcomes. Frontiers in Immunology, v. 8, p. 542, 2017.1664-3224https://www.arca.fiocruz.br/handle/icict/2555610.3389/fimmu.2017.00542Intramural Research Program of the NIAID and by a grant from the National Institutes of Health (NIH) U01AI115940. RW is supported by the Francis Crick Institute which receives its core funding from Câncer Research UK (FC00110218), the UK Medical Research CouncilUniversity of Cape Town. Institute of Infectious Disease and Molecular Medicine. Wellcome Centre for Infectious Disease Research in Africa. Cape Town, South Africa / Imperial College. Department of Medicine. London, UKNational Institutes of Health. National Institutes of Allergy and Infectious Diseases. Laboratory of Parasitic Diseases. Immunobiology Section. Bethesda, MD, USANational Institutes of Health. National Institutes of Allergy and Infectious Diseases. Laboratory of Parasitic Diseases. Immunobiology Section. Bethesda, MD, USAUniversity of Cape Town. Institute of Infectious Disease and Molecular Medicine. Wellcome Centre for Infectious Disease Research in Africa. Cape Town, South AfricaImperial College. Infectious Diseases and Immunity. London, UK / Johns Hopkins University School of Medicine. Center for Tuberculosis Research. Baltimore, MD, USAFundação Oswaldo Cruz. Instituto Gonçalo Moniz. Salvador, BA, Brasil / Initiative Fundação José Silveira. Multinational Organization Network Sponsoring Translational and Epidemiological Research. Salvador, BA, Brazil / Faculdade de Tecnologia e Ciências,Curso de Medicina. Salvador, BA, BrasilFundação Oswaldo Cruz. Instituto Gonçalo Moniz. Salvador, BA, BrasilUniversity of Pittsburgh School of Medicine. Department of Microbiology and Molecular Genetics. Pittsburgh, PA, USAUniversity of Pittsburgh School of Medicine. Department of Microbiology and Molecular Genetics. Pittsburgh, PA, USANational Institutes of Health. National Institute on Minority Health and Health Disparities. Division of Intramural Research. Bethesda, MD, USAUniversity of Cape Town. Institute of Infectious Disease and Molecular Medicine. Wellcome Centre for Infectious Disease Research in Africa. Cape Town, South Africa / The Francis Crick Institute. London, UKJohns Hopkins University School of Medicine. Center for Tuberculosis Research. Baltimore, MD, USANational Institutes of Health. National Institutes of Allergy and Infectious Diseases. Laboratory of Parasitic Diseases. Immunobiology Section. Bethesda, MD, USAUniversity of Cape Town. Institute of Infectious Disease and Molecular Medicine. Wellcome Centre for Infectious Disease Research in Africa. Cape Town, South Africa / Imperial College. Department of Medicine. London, UK / The Francis Crick Institute. London, UKUniversity of Cape Town. Institute of Infectious Disease and Molecular Medicine. Wellcome Centre for Infectious Disease Research in Africa. Cape Town, South Africa / Fundação Oswaldo Cruz. Instituto Gonçalo Moniz. Salvador, BA, Brasil / Initiative Fundação José Silveira. Multinational Organization Network Sponsoring Translational and Epidemiological Research. Salvador, BA, Brazil / Faculdade de Tecnologia e Ciências,Curso de Medicina. Salvador, BA, Brasil / Vanderbilt University School of Medicine. Division of Infectious Diseases. Department of Medicine. Nashville, TN, USA / Escola Bahiana de Medicina e Saúde Pública. Salvador, BA, BrasilThe antioxidant enzyme heme oxygenase-1 (HO-1) is implicated in the pathogenesis of tuberculosis (TB) and has been proposed as a biomarker of active disease. Nevertheless, the mechanisms by whichMycobacterium tuberculosis(Mtb) induces HO-1 as well as how its expression is affected by HIV-1 coinfection and successful antitubercular therapy (ATT) are poorly understood. We found that HO-1 expression is markedly increased in rabbits, mice, and non-human primates during experimentalMtbinfection and gradually decreased during ATT. In addition, we examined circulating concentrations of HO-1 in a cohort of 130 HIV-1 coinfected and uninfected pulmonary TB patients undergoing ATT to investigate changes in expression of this biomarker in relation to HIV-1 status, radiological disease severity, and treatment outcome. We found that plasma levels of HO-1 were elevated in untreated HIV-1 coinfected TB patients and correlated positively with HIV-1 viral load and negatively with CD4+T cell count. In both HIV-1 coinfected andMtbmonoinfected patients, HO-1 levels were substantially reduced during successful TB treatment but not in those who experienced treatment failure or subsequently relapsed. To further delineate the molecular mechanisms involved in induction of HO-1 byMtb, we performed a series ofin vitroexperiments using mouse and human macrophages. We found thatMtb-induced HO-1 expression requires NADPH oxidase-dependent reactive oxygen species production induced by the early-secreted antigen ESAT-6, which in turn triggers nuclear translocation of the transcription factor NRF-2. These observations provide further insight into the utility of HO-1 as a biomarker of both disease and successful therapy in TB monoinfected and HIV-TB coinfected patients and reveal a previously undocumented pathway linking expression of the enzyme with oxidative stress.engFrontiers MediaTuberculoseHIVHeme oxigenase-1BiomarcadorEstresse oxidativoTuberculosisHIVHeme oxygenase-1BiomarkerOxidative stressMycobacterium tuberculosisInduction of Heme Oxygenase-1 Expression Is Dependent on Oxidative Stress and Reflects Treatment Outcomesinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da FIOCRUZ (ARCA)instname:Fundação Oswaldo Cruz (FIOCRUZ)instacron:FIOCRUZLICENSElicense.txtlicense.txttext/plain; charset=utf-82991https://www.arca.fiocruz.br/bitstream/icict/25556/1/license.txt5a560609d32a3863062d77ff32785d58MD51ORIGINALRockwood N Mycobacterium tuberculosis Induction ....pdfRockwood N Mycobacterium 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dc.title.pt_BR.fl_str_mv Mycobacterium tuberculosisInduction of Heme Oxygenase-1 Expression Is Dependent on Oxidative Stress and Reflects Treatment Outcomes
title Mycobacterium tuberculosisInduction of Heme Oxygenase-1 Expression Is Dependent on Oxidative Stress and Reflects Treatment Outcomes
spellingShingle Mycobacterium tuberculosisInduction of Heme Oxygenase-1 Expression Is Dependent on Oxidative Stress and Reflects Treatment Outcomes
Rockwood, Neesha
Tuberculose
HIV
Heme oxigenase-1
Biomarcador
Estresse oxidativo
Tuberculosis
HIV
Heme oxygenase-1
Biomarker
Oxidative stress
title_short Mycobacterium tuberculosisInduction of Heme Oxygenase-1 Expression Is Dependent on Oxidative Stress and Reflects Treatment Outcomes
title_full Mycobacterium tuberculosisInduction of Heme Oxygenase-1 Expression Is Dependent on Oxidative Stress and Reflects Treatment Outcomes
title_fullStr Mycobacterium tuberculosisInduction of Heme Oxygenase-1 Expression Is Dependent on Oxidative Stress and Reflects Treatment Outcomes
title_full_unstemmed Mycobacterium tuberculosisInduction of Heme Oxygenase-1 Expression Is Dependent on Oxidative Stress and Reflects Treatment Outcomes
title_sort Mycobacterium tuberculosisInduction of Heme Oxygenase-1 Expression Is Dependent on Oxidative Stress and Reflects Treatment Outcomes
author Rockwood, Neesha
author_facet Rockwood, Neesha
Costa, Diego Luis
Amaral, Eduardo Pinheiro
Du Bruyn, Elsa
Kubler, Andre
Gil-Santana, Leonardo
Fukutani, Kiyoshi F
Scanga, Charles A
Flynn, JoAnne L
Jackson, Sharon H
Wilkinson, Katalin A
Bishai, William R
Sher, Alan
Wilkinson, Robert J
Andrade, Bruno de Bezerril
author_role author
author2 Costa, Diego Luis
Amaral, Eduardo Pinheiro
Du Bruyn, Elsa
Kubler, Andre
Gil-Santana, Leonardo
Fukutani, Kiyoshi F
Scanga, Charles A
Flynn, JoAnne L
Jackson, Sharon H
Wilkinson, Katalin A
Bishai, William R
Sher, Alan
Wilkinson, Robert J
Andrade, Bruno de Bezerril
author2_role author
author
author
author
author
author
author
author
author
author
author
author
author
author
dc.contributor.author.fl_str_mv Rockwood, Neesha
Costa, Diego Luis
Amaral, Eduardo Pinheiro
Du Bruyn, Elsa
Kubler, Andre
Gil-Santana, Leonardo
Fukutani, Kiyoshi F
Scanga, Charles A
Flynn, JoAnne L
Jackson, Sharon H
Wilkinson, Katalin A
Bishai, William R
Sher, Alan
Wilkinson, Robert J
Andrade, Bruno de Bezerril
dc.subject.other.pt_BR.fl_str_mv Tuberculose
HIV
Heme oxigenase-1
Biomarcador
Estresse oxidativo
topic Tuberculose
HIV
Heme oxigenase-1
Biomarcador
Estresse oxidativo
Tuberculosis
HIV
Heme oxygenase-1
Biomarker
Oxidative stress
dc.subject.en.pt_BR.fl_str_mv Tuberculosis
HIV
Heme oxygenase-1
Biomarker
Oxidative stress
description Intramural Research Program of the NIAID and by a grant from the National Institutes of Health (NIH) U01AI115940. RW is supported by the Francis Crick Institute which receives its core funding from Câncer Research UK (FC00110218), the UK Medical Research Council
publishDate 2017
dc.date.issued.fl_str_mv 2017
dc.date.accessioned.fl_str_mv 2018-04-02T14:08:02Z
dc.date.available.fl_str_mv 2018-04-02T14:08:02Z
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
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status_str publishedVersion
dc.identifier.citation.fl_str_mv ROCKWOOD, N. et al. Mycobacterium tuberculosisInduction of Heme Oxygenase-1 Expression Is Dependent on Oxidative Stress and Reflects Treatment Outcomes. Frontiers in Immunology, v. 8, p. 542, 2017.
dc.identifier.uri.fl_str_mv https://www.arca.fiocruz.br/handle/icict/25556
dc.identifier.issn.pt_BR.fl_str_mv 1664-3224
dc.identifier.doi.none.fl_str_mv 10.3389/fimmu.2017.00542
identifier_str_mv ROCKWOOD, N. et al. Mycobacterium tuberculosisInduction of Heme Oxygenase-1 Expression Is Dependent on Oxidative Stress and Reflects Treatment Outcomes. Frontiers in Immunology, v. 8, p. 542, 2017.
1664-3224
10.3389/fimmu.2017.00542
url https://www.arca.fiocruz.br/handle/icict/25556
dc.language.iso.fl_str_mv eng
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dc.publisher.none.fl_str_mv Frontiers Media
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