Joint NOD2/RIPK2 signaling regulates IL-17 axis and contributes to the development of experimental arthritis

Detalhes bibliográficos
Autor(a) principal: Manfredo Vieira, Silvio
Data de Publicação: 2012
Outros Autores: Cunha, Thiago Mattar, França, Rafael Freitas de Oliveira, Pinto, Larissa Garcia, Talbot, Jhimmy, Turato, Walter Miguel, Lemos, Henrique Paula, Lima, Jonilson Berlink, Verri, Waldiceu A., Almeida, Sërgio C.L., Ferreira, Seérgio Henrique, Louzada-Jünior, Paulo, Zamboni, Darío Simões, Cunha, Fernando Queiroz
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional do INPA
Texto Completo: https://repositorio.inpa.gov.br/handle/1/16128
Resumo: Intracellular pattern recognition receptors such as the nucleotide-binding oligomerization domain (NOD)-like receptors family members are key for innate immune recognition of microbial infection and may play important roles in the development of inflammatory diseases, including rheumatic diseases. In this study, we evaluated the role of NOD1 and NOD2 on development of experimental arthritis. Ag-induced arthritis was generated in wild-type, NOD1 -/-, NOD2 -/-, or receptor-interacting serine-threonine kinase 2 -/- (RIPK2 -/-) immunized mice challenged intra-articularly with methylated BSA. Nociception was determined by electronic Von Frey test. Neutrophil recruitment and histopathological analysis of proteoglycan lost was evaluated in inflamed joints. Joint levels of inflammatory cytokine/chemokine were measured by ELISA. Cytokine (IL-6 and IL-23) and NOD2 expressions were determined in mice synovial tissue by RT-PCR. The NOD2 -/- and RIPK2 -/-, but not NOD1 -/-, mice are protected from Ag-induced arthritis, which was characterized by a reduction in neutrophil recruitment, nociception, and cartilage degradation. NOD2/RIPK2 signaling impairment was associated with a reduction in proinflammatory cytokines and chemokines (TNF, IL-1b, and CXCL1/KC). IL-17 and IL-17 triggering cytokines (IL-6 and IL-23) were also reduced in the joint, but there is no difference in the percentage of CD4 + IL-17 + cells in the lymph node between arthritic wild-type and NOD2 -/- mice. Altogether, these findings point to a pivotal role of the NOD2/RIPK2 signaling in the onset of experimental arthritis by triggering an IL-17-dependent joint immune response. Therefore, we could propose that NOD2 signaling is a target for the development of new therapies for the control of rheumatoid arthritis. Copyright © 2012 by The American Association of Immunologists, Inc.
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spelling Manfredo Vieira, SilvioCunha, Thiago MattarFrança, Rafael Freitas de OliveiraPinto, Larissa GarciaTalbot, JhimmyTurato, Walter MiguelLemos, Henrique PaulaLima, Jonilson BerlinkVerri, Waldiceu A.Almeida, Sërgio C.L.Ferreira, Seérgio HenriqueLouzada-Jünior, PauloZamboni, Darío SimõesCunha, Fernando Queiroz2020-05-24T22:15:12Z2020-05-24T22:15:12Z2012https://repositorio.inpa.gov.br/handle/1/1612810.4049/jimmunol.1004190Intracellular pattern recognition receptors such as the nucleotide-binding oligomerization domain (NOD)-like receptors family members are key for innate immune recognition of microbial infection and may play important roles in the development of inflammatory diseases, including rheumatic diseases. In this study, we evaluated the role of NOD1 and NOD2 on development of experimental arthritis. Ag-induced arthritis was generated in wild-type, NOD1 -/-, NOD2 -/-, or receptor-interacting serine-threonine kinase 2 -/- (RIPK2 -/-) immunized mice challenged intra-articularly with methylated BSA. Nociception was determined by electronic Von Frey test. Neutrophil recruitment and histopathological analysis of proteoglycan lost was evaluated in inflamed joints. Joint levels of inflammatory cytokine/chemokine were measured by ELISA. Cytokine (IL-6 and IL-23) and NOD2 expressions were determined in mice synovial tissue by RT-PCR. The NOD2 -/- and RIPK2 -/-, but not NOD1 -/-, mice are protected from Ag-induced arthritis, which was characterized by a reduction in neutrophil recruitment, nociception, and cartilage degradation. NOD2/RIPK2 signaling impairment was associated with a reduction in proinflammatory cytokines and chemokines (TNF, IL-1b, and CXCL1/KC). IL-17 and IL-17 triggering cytokines (IL-6 and IL-23) were also reduced in the joint, but there is no difference in the percentage of CD4 + IL-17 + cells in the lymph node between arthritic wild-type and NOD2 -/- mice. Altogether, these findings point to a pivotal role of the NOD2/RIPK2 signaling in the onset of experimental arthritis by triggering an IL-17-dependent joint immune response. Therefore, we could propose that NOD2 signaling is a target for the development of new therapies for the control of rheumatoid arthritis. Copyright © 2012 by The American Association of Immunologists, Inc.Volume 188, Número 10, Pags. 5116-5122Attribution-NonCommercial-NoDerivs 3.0 Brazilhttp://creativecommons.org/licenses/by-nc-nd/3.0/br/info:eu-repo/semantics/openAccessCaspase Recruitment Domain Protein 15Caspase Recruitment Domain Protein 4Cd4 AntigenCxcl1 ChemokineInterleukin-17Interleukin-1betaInterleukin-23Interleukin-6ProteoglycanReceptor Interacting Protein Serine Threonine Kinase 2Tumor Necrosis FactorAnimals CellAnimals ExperimentAnimals ModelAnimals TissueArthritisCartilage DegenerationControlled StudyEnzyme ActivityEnzyme-linked Immunosorbent AssayEnzyme RegulationHistopathologyImmune ResponseMouseNeutrophilNociceptionNonhumanPriority JournalProtein ExpressionProtein FunctionReverse Transcription Polymerase Chain ReactionArthritis, RheumatoidSignal TransductionSynoviumAnimalArthritis, ExperimentalCattleCells, CulturedInterleukin-17Knee JointMiceMice, Inbred C57blMice, KnockoutNod1 Signaling Adaptor ProteinNod2 Signaling Adaptor ProteinReceptor-interacting Protein Serine-threonine KinasesSerum Albumin, BovineSignal TransductionJoint NOD2/RIPK2 signaling regulates IL-17 axis and contributes to the development of experimental arthritisinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleJournal of Immunologyengreponame:Repositório Institucional do INPAinstname:Instituto Nacional de Pesquisas da Amazônia (INPA)instacron:INPAORIGINALartigo-inpa.pdfartigo-inpa.pdfapplication/pdf1157744https://repositorio.inpa.gov.br/bitstream/1/16128/1/artigo-inpa.pdfd8910ab242dcfa09d90bd3ae97928cbaMD511/161282020-05-25 10:25:15.089oai:repositorio:1/16128Repositório de PublicaçõesPUBhttps://repositorio.inpa.gov.br/oai/requestopendoar:2020-05-25T14:25:15Repositório Institucional do INPA - Instituto Nacional de Pesquisas da Amazônia (INPA)false
dc.title.en.fl_str_mv Joint NOD2/RIPK2 signaling regulates IL-17 axis and contributes to the development of experimental arthritis
title Joint NOD2/RIPK2 signaling regulates IL-17 axis and contributes to the development of experimental arthritis
spellingShingle Joint NOD2/RIPK2 signaling regulates IL-17 axis and contributes to the development of experimental arthritis
Manfredo Vieira, Silvio
Caspase Recruitment Domain Protein 15
Caspase Recruitment Domain Protein 4
Cd4 Antigen
Cxcl1 Chemokine
Interleukin-17
Interleukin-1beta
Interleukin-23
Interleukin-6
Proteoglycan
Receptor Interacting Protein Serine Threonine Kinase 2
Tumor Necrosis Factor
Animals Cell
Animals Experiment
Animals Model
Animals Tissue
Arthritis
Cartilage Degeneration
Controlled Study
Enzyme Activity
Enzyme-linked Immunosorbent Assay
Enzyme Regulation
Histopathology
Immune Response
Mouse
Neutrophil
Nociception
Nonhuman
Priority Journal
Protein Expression
Protein Function
Reverse Transcription Polymerase Chain Reaction
Arthritis, Rheumatoid
Signal Transduction
Synovium
Animal
Arthritis, Experimental
Cattle
Cells, Cultured
Interleukin-17
Knee Joint
Mice
Mice, Inbred C57bl
Mice, Knockout
Nod1 Signaling Adaptor Protein
Nod2 Signaling Adaptor Protein
Receptor-interacting Protein Serine-threonine Kinases
Serum Albumin, Bovine
Signal Transduction
title_short Joint NOD2/RIPK2 signaling regulates IL-17 axis and contributes to the development of experimental arthritis
title_full Joint NOD2/RIPK2 signaling regulates IL-17 axis and contributes to the development of experimental arthritis
title_fullStr Joint NOD2/RIPK2 signaling regulates IL-17 axis and contributes to the development of experimental arthritis
title_full_unstemmed Joint NOD2/RIPK2 signaling regulates IL-17 axis and contributes to the development of experimental arthritis
title_sort Joint NOD2/RIPK2 signaling regulates IL-17 axis and contributes to the development of experimental arthritis
author Manfredo Vieira, Silvio
author_facet Manfredo Vieira, Silvio
Cunha, Thiago Mattar
França, Rafael Freitas de Oliveira
Pinto, Larissa Garcia
Talbot, Jhimmy
Turato, Walter Miguel
Lemos, Henrique Paula
Lima, Jonilson Berlink
Verri, Waldiceu A.
Almeida, Sërgio C.L.
Ferreira, Seérgio Henrique
Louzada-Jünior, Paulo
Zamboni, Darío Simões
Cunha, Fernando Queiroz
author_role author
author2 Cunha, Thiago Mattar
França, Rafael Freitas de Oliveira
Pinto, Larissa Garcia
Talbot, Jhimmy
Turato, Walter Miguel
Lemos, Henrique Paula
Lima, Jonilson Berlink
Verri, Waldiceu A.
Almeida, Sërgio C.L.
Ferreira, Seérgio Henrique
Louzada-Jünior, Paulo
Zamboni, Darío Simões
Cunha, Fernando Queiroz
author2_role author
author
author
author
author
author
author
author
author
author
author
author
author
dc.contributor.author.fl_str_mv Manfredo Vieira, Silvio
Cunha, Thiago Mattar
França, Rafael Freitas de Oliveira
Pinto, Larissa Garcia
Talbot, Jhimmy
Turato, Walter Miguel
Lemos, Henrique Paula
Lima, Jonilson Berlink
Verri, Waldiceu A.
Almeida, Sërgio C.L.
Ferreira, Seérgio Henrique
Louzada-Jünior, Paulo
Zamboni, Darío Simões
Cunha, Fernando Queiroz
dc.subject.eng.fl_str_mv Caspase Recruitment Domain Protein 15
Caspase Recruitment Domain Protein 4
Cd4 Antigen
Cxcl1 Chemokine
Interleukin-17
Interleukin-1beta
Interleukin-23
Interleukin-6
Proteoglycan
Receptor Interacting Protein Serine Threonine Kinase 2
Tumor Necrosis Factor
Animals Cell
Animals Experiment
Animals Model
Animals Tissue
Arthritis
Cartilage Degeneration
Controlled Study
Enzyme Activity
Enzyme-linked Immunosorbent Assay
Enzyme Regulation
Histopathology
Immune Response
Mouse
Neutrophil
Nociception
Nonhuman
Priority Journal
Protein Expression
Protein Function
Reverse Transcription Polymerase Chain Reaction
Arthritis, Rheumatoid
Signal Transduction
Synovium
Animal
Arthritis, Experimental
Cattle
Cells, Cultured
Interleukin-17
Knee Joint
Mice
Mice, Inbred C57bl
Mice, Knockout
Nod1 Signaling Adaptor Protein
Nod2 Signaling Adaptor Protein
Receptor-interacting Protein Serine-threonine Kinases
Serum Albumin, Bovine
Signal Transduction
topic Caspase Recruitment Domain Protein 15
Caspase Recruitment Domain Protein 4
Cd4 Antigen
Cxcl1 Chemokine
Interleukin-17
Interleukin-1beta
Interleukin-23
Interleukin-6
Proteoglycan
Receptor Interacting Protein Serine Threonine Kinase 2
Tumor Necrosis Factor
Animals Cell
Animals Experiment
Animals Model
Animals Tissue
Arthritis
Cartilage Degeneration
Controlled Study
Enzyme Activity
Enzyme-linked Immunosorbent Assay
Enzyme Regulation
Histopathology
Immune Response
Mouse
Neutrophil
Nociception
Nonhuman
Priority Journal
Protein Expression
Protein Function
Reverse Transcription Polymerase Chain Reaction
Arthritis, Rheumatoid
Signal Transduction
Synovium
Animal
Arthritis, Experimental
Cattle
Cells, Cultured
Interleukin-17
Knee Joint
Mice
Mice, Inbred C57bl
Mice, Knockout
Nod1 Signaling Adaptor Protein
Nod2 Signaling Adaptor Protein
Receptor-interacting Protein Serine-threonine Kinases
Serum Albumin, Bovine
Signal Transduction
description Intracellular pattern recognition receptors such as the nucleotide-binding oligomerization domain (NOD)-like receptors family members are key for innate immune recognition of microbial infection and may play important roles in the development of inflammatory diseases, including rheumatic diseases. In this study, we evaluated the role of NOD1 and NOD2 on development of experimental arthritis. Ag-induced arthritis was generated in wild-type, NOD1 -/-, NOD2 -/-, or receptor-interacting serine-threonine kinase 2 -/- (RIPK2 -/-) immunized mice challenged intra-articularly with methylated BSA. Nociception was determined by electronic Von Frey test. Neutrophil recruitment and histopathological analysis of proteoglycan lost was evaluated in inflamed joints. Joint levels of inflammatory cytokine/chemokine were measured by ELISA. Cytokine (IL-6 and IL-23) and NOD2 expressions were determined in mice synovial tissue by RT-PCR. The NOD2 -/- and RIPK2 -/-, but not NOD1 -/-, mice are protected from Ag-induced arthritis, which was characterized by a reduction in neutrophil recruitment, nociception, and cartilage degradation. NOD2/RIPK2 signaling impairment was associated with a reduction in proinflammatory cytokines and chemokines (TNF, IL-1b, and CXCL1/KC). IL-17 and IL-17 triggering cytokines (IL-6 and IL-23) were also reduced in the joint, but there is no difference in the percentage of CD4 + IL-17 + cells in the lymph node between arthritic wild-type and NOD2 -/- mice. Altogether, these findings point to a pivotal role of the NOD2/RIPK2 signaling in the onset of experimental arthritis by triggering an IL-17-dependent joint immune response. Therefore, we could propose that NOD2 signaling is a target for the development of new therapies for the control of rheumatoid arthritis. Copyright © 2012 by The American Association of Immunologists, Inc.
publishDate 2012
dc.date.issued.fl_str_mv 2012
dc.date.accessioned.fl_str_mv 2020-05-24T22:15:12Z
dc.date.available.fl_str_mv 2020-05-24T22:15:12Z
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv https://repositorio.inpa.gov.br/handle/1/16128
dc.identifier.doi.none.fl_str_mv 10.4049/jimmunol.1004190
url https://repositorio.inpa.gov.br/handle/1/16128
identifier_str_mv 10.4049/jimmunol.1004190
dc.language.iso.fl_str_mv eng
language eng
dc.relation.ispartof.pt_BR.fl_str_mv Volume 188, Número 10, Pags. 5116-5122
dc.rights.driver.fl_str_mv Attribution-NonCommercial-NoDerivs 3.0 Brazil
http://creativecommons.org/licenses/by-nc-nd/3.0/br/
info:eu-repo/semantics/openAccess
rights_invalid_str_mv Attribution-NonCommercial-NoDerivs 3.0 Brazil
http://creativecommons.org/licenses/by-nc-nd/3.0/br/
eu_rights_str_mv openAccess
dc.publisher.none.fl_str_mv Journal of Immunology
publisher.none.fl_str_mv Journal of Immunology
dc.source.none.fl_str_mv reponame:Repositório Institucional do INPA
instname:Instituto Nacional de Pesquisas da Amazônia (INPA)
instacron:INPA
instname_str Instituto Nacional de Pesquisas da Amazônia (INPA)
instacron_str INPA
institution INPA
reponame_str Repositório Institucional do INPA
collection Repositório Institucional do INPA
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