RIPK1 and PGAM5 Control Leishmania Replication through Distinct Mechanisms
| Autor(a) principal: | |
|---|---|
| Data de Publicação: | 2016 |
| Outros Autores: | , , , , , , , , , |
| Tipo de documento: | Artigo |
| Idioma: | eng |
| Título da fonte: | Repositório Institucional da FIOCRUZ (ARCA) |
| Texto Completo: | https://www.arca.fiocruz.br/handle/icict/18872 |
Resumo: | National Institutes of Health Grant AI119030 (to F.K.-M.C.), the Fundação de Amparo à Pesquisa do Estado da Bahia (to V.M.B.), and a postdoctoral fellowship from Conselho Nacional de Desenvolvimento Científico e Tecnológico (to N.F.L.). |
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Luz, Nivea FariasBalaji, SakthiOkuda, KendiBarreto, Aline SilvaBertin, JohnGough, Peter JGazzinelli, Ricardo TostesAlmeida, Roque Pacheco deBozza, Marcelo TorresBorges, Valeria de MatosChan, Francis Ka-Ming2017-05-16T17:24:36Z2017-05-16T17:24:36Z2016LUZ, N. F. et al. RIPK1 and PGAM5 Control Leishmania Replication through Distinct Mechanisms. The Journal of Immunology, v. 196, 2016.0022-1767https://www.arca.fiocruz.br/handle/icict/1887210.4049/jimmunol.1502492National Institutes of Health Grant AI119030 (to F.K.-M.C.), the Fundação de Amparo à Pesquisa do Estado da Bahia (to V.M.B.), and a postdoctoral fellowship from Conselho Nacional de Desenvolvimento Científico e Tecnológico (to N.F.L.).University of Massachusetts Medical School. Department of Pathology. Worcester, MA / Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, BrasilUniversity of Massachusetts Medical School. Department of Pathology. Worcester, MAUniversity of Massachusetts Medical School. Division of Infectious Diseases and Immunology. Worcester, MAUniversidade Federal de Sergipe. Hospital Universitário. Departamento de Medicina. Aracaju, SE, BrasilFundação Oswaldo Cruz. Centro de Pesquisa Rene Rachou. Laboratorio de Imunopatologia. Belo Horizonte, MG, BrasilPattern Recognition Receptor Discovery Performance Unit. Immuno-Inflammation Therapeutic Area, GlaxoSmithKline. Collegeville, PAUniversity of Massachusetts Medical School. Division of Infectious Diseases and Immunology. Worcester, MA / Fundação Oswaldo Cruz. Centro de Pesquisa Rene Rachou. Laboratorio de Imunopatologia. Belo Horizonte, MG, BrasilUniversidade Federal de Sergipe. Hospital Universitário. Departamento de Medicina. Aracaju, SE, BrasilUniversidade Federal do Rio de Janeiro. Instituto de Microbiologia. Departamento de Imunologia, Rio de Janeiro, RJ, BrasilFundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, BrasilUniversity of Massachusetts Medical School. Immunology and Microbiology Program. Worcester, MA / University of Massachusetts Medical School. Department of Pathology. Worcester, MALeishmaniasis is an important parasitic disease found in the tropics and subtropics. Cutaneous and visceral leishmaniasis affect an estimated 1.5 million people worldwide. Despite its human health relevance, relatively little is known about the cell death pathways that control Leishmania replication in the host. Necroptosis is a recently identified form of cell death with potent antiviral effects. Receptor interacting protein kinase 1 (RIPK1) is a critical kinase that mediates necroptosis downstream of death receptors and TLRs. Heme, a product of hemoglobin catabolism during certain intracellular pathogen infections, is also a potent inducer of macrophage necroptosis. We found that human visceral leishmaniasis patients exhibit elevated serum levels of heme. Therefore, we examined the impact of heme and necroptosis on Leishmania replication. Indeed, heme potently inhibited Leishmania replication in bone marrow-derived macrophages. Moreover, we found that inhibition of RIPK1 kinase activity also enhanced parasite replication in the absence of heme. We further found that the mitochondrial phosphatase phosphoglycerate mutase family member 5 (PGAM5), a putative downstream effector of RIPK1, was also required for inhibition of Leishmania replication. In mouse infection, both PGAM5 and RIPK1 kinase activity are required for IL-1β expression in response to Leishmania However, PGAM5, but not RIPK1 kinase activity, was directly responsible for Leishmania-induced IL-1β secretion and NO production in bone marrow-derived macrophages. Collectively, these results revealed that RIPK1 and PGAM5 function independently to exert optimal control of Leishmania replication in the host.engAmerican Association of Immunologists, Inc.LeishmaniaLeishmaniose CutâneaMorte celularProteína quinaseHemeMedula ósseaMacrófagosLeishmaniaLeishmaniasis, CutaneousCell deathProtein kinaseHemeBone marrowMacrophagesLeishmaniaLeishmaniose CutaneaMorte celularKinaseMedula ósseaHemeMacrófagosRIPK1 and PGAM5 Control Leishmania Replication through Distinct Mechanismsinfo: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/18872/1/license.txt5a560609d32a3863062d77ff32785d58MD51ORIGINALLuz NF RIPK1 and PGAM5 control leishmania....pdfLuz NF RIPK1 and PGAM5 control 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| dc.title.pt_BR.fl_str_mv |
RIPK1 and PGAM5 Control Leishmania Replication through Distinct Mechanisms |
| title |
RIPK1 and PGAM5 Control Leishmania Replication through Distinct Mechanisms |
| spellingShingle |
RIPK1 and PGAM5 Control Leishmania Replication through Distinct Mechanisms Luz, Nivea Farias Leishmania Leishmaniose Cutânea Morte celular Proteína quinase Heme Medula óssea Macrófagos Leishmania Leishmaniasis, Cutaneous Cell death Protein kinase Heme Bone marrow Macrophages Leishmania Leishmaniose Cutanea Morte celular Kinase Medula óssea Heme Macrófagos |
| title_short |
RIPK1 and PGAM5 Control Leishmania Replication through Distinct Mechanisms |
| title_full |
RIPK1 and PGAM5 Control Leishmania Replication through Distinct Mechanisms |
| title_fullStr |
RIPK1 and PGAM5 Control Leishmania Replication through Distinct Mechanisms |
| title_full_unstemmed |
RIPK1 and PGAM5 Control Leishmania Replication through Distinct Mechanisms |
| title_sort |
RIPK1 and PGAM5 Control Leishmania Replication through Distinct Mechanisms |
| author |
Luz, Nivea Farias |
| author_facet |
Luz, Nivea Farias Balaji, Sakthi Okuda, Kendi Barreto, Aline Silva Bertin, John Gough, Peter J Gazzinelli, Ricardo Tostes Almeida, Roque Pacheco de Bozza, Marcelo Torres Borges, Valeria de Matos Chan, Francis Ka-Ming |
| author_role |
author |
| author2 |
Balaji, Sakthi Okuda, Kendi Barreto, Aline Silva Bertin, John Gough, Peter J Gazzinelli, Ricardo Tostes Almeida, Roque Pacheco de Bozza, Marcelo Torres Borges, Valeria de Matos Chan, Francis Ka-Ming |
| author2_role |
author author author author author author author author author author |
| dc.contributor.author.fl_str_mv |
Luz, Nivea Farias Balaji, Sakthi Okuda, Kendi Barreto, Aline Silva Bertin, John Gough, Peter J Gazzinelli, Ricardo Tostes Almeida, Roque Pacheco de Bozza, Marcelo Torres Borges, Valeria de Matos Chan, Francis Ka-Ming |
| dc.subject.other.pt_BR.fl_str_mv |
Leishmania Leishmaniose Cutânea Morte celular Proteína quinase Heme Medula óssea Macrófagos |
| topic |
Leishmania Leishmaniose Cutânea Morte celular Proteína quinase Heme Medula óssea Macrófagos Leishmania Leishmaniasis, Cutaneous Cell death Protein kinase Heme Bone marrow Macrophages Leishmania Leishmaniose Cutanea Morte celular Kinase Medula óssea Heme Macrófagos |
| dc.subject.en.pt_BR.fl_str_mv |
Leishmania Leishmaniasis, Cutaneous Cell death Protein kinase Heme Bone marrow Macrophages |
| dc.subject.decs.pt_BR.fl_str_mv |
Leishmania Leishmaniose Cutanea Morte celular Kinase Medula óssea Heme Macrófagos |
| description |
National Institutes of Health Grant AI119030 (to F.K.-M.C.), the Fundação de Amparo à Pesquisa do Estado da Bahia (to V.M.B.), and a postdoctoral fellowship from Conselho Nacional de Desenvolvimento Científico e Tecnológico (to N.F.L.). |
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2016 |
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2016 |
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2017-05-16T17:24:36Z |
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2017-05-16T17:24:36Z |
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info:eu-repo/semantics/publishedVersion |
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info:eu-repo/semantics/article |
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article |
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publishedVersion |
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LUZ, N. F. et al. RIPK1 and PGAM5 Control Leishmania Replication through Distinct Mechanisms. The Journal of Immunology, v. 196, 2016. |
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https://www.arca.fiocruz.br/handle/icict/18872 |
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0022-1767 |
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10.4049/jimmunol.1502492 |
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LUZ, N. F. et al. RIPK1 and PGAM5 Control Leishmania Replication through Distinct Mechanisms. The Journal of Immunology, v. 196, 2016. 0022-1767 10.4049/jimmunol.1502492 |
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American Association of Immunologists, Inc. |
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American Association of Immunologists, Inc. |
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