Modulation of Lung Allergic Response by Renal Ischemia and Reperfusion Injury

Detalhes bibliográficos
Autor(a) principal: Campanholle, Gabriela
Data de Publicação: 2012
Outros Autores: Silva, Reinaldo Correia [UNIFESP], Martins, Joilson O., Landgraf, Maristella A., Paiva, Vanessa N., Ferreira, Renaide Rodrigues [UNIFESP], Amano, Mariane T., Hiyane, Meire Ioshie [UNIFESP], Cenedeze, Marcos Antonio [UNIFESP], Pacheco-Silva, Alvaro [UNIFESP], Camara, Niels Olsen Saraiva [UNIFESP], Landgraf, Richardt Gama [UNIFESP]
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UNIFESP
Texto Completo: http://repositorio.unifesp.br/handle/11600/34385
http://dx.doi.org/10.1159/000338506
Resumo: The Th1/Th2 balance represents an important factor in the pathogenesis of renal ischemia-reperfusion injury (IRI). in addition, IRI causes a systemic inflammation that can affect other tissues, such as the lungs. To investigate the ability of renal IRI to modulate pulmonary function in a specific model of allergic inflammation, C57Bl/6 mice were immunized with ovalbumin/albumen on days 0 and 7 and challenged with an ovalbumin (OA) aerosol on days 14 and 21. After 24 h of the second antigen challenge, the animals were subjected to 45 minutes of ischemia. After 24 h of reperfusion, the bronchoalveolar lavage (BAL) fluid, blood and lung tissue were collected for analysis. Serum creatinine levels increased in both allergic and non-immunized animals subjected to IRI. However, BAL analysis showed a reduction in the total cells (46%) and neutrophils (58%) compared with control allergic animals not submitted to IRI. in addition, OA challenge induced the phosphorylation of ERK and Akt and the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in lung homogenates. After renal IRI, the phosphorylation of ERK and expression of COX-2 and iNOS were markedly reduced; however, there was no difference in the phosphorylation of Akt between sham and ischemic OA-challenged animals. Mucus production was also reduced in allergic mice after renal IRI. IL-4, IL-5 and IL-13 were markedly down-regulated in immunized/challenged mice subjected to IRI. These results suggest that renal IRI can modulate lung allergic inflammation, probably by altering the Th1/Th2 balance and, at least in part, by changing cellular signal transduction factors. Copyright (C) 2012 S. Karger AG, Basel
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spelling Campanholle, GabrielaSilva, Reinaldo Correia [UNIFESP]Martins, Joilson O.Landgraf, Maristella A.Paiva, Vanessa N.Ferreira, Renaide Rodrigues [UNIFESP]Amano, Mariane T.Hiyane, Meire Ioshie [UNIFESP]Cenedeze, Marcos Antonio [UNIFESP]Pacheco-Silva, Alvaro [UNIFESP]Camara, Niels Olsen Saraiva [UNIFESP]Landgraf, Richardt Gama [UNIFESP]Universidade Federal de São Paulo (UNIFESP)Universidade de São Paulo (USP)2016-01-24T14:17:38Z2016-01-24T14:17:38Z2012-01-01Cellular Physiology and Biochemistry. Basel: Karger, v. 29, n. 3-4, p. 523-532, 2012.1015-8987http://repositorio.unifesp.br/handle/11600/34385http://dx.doi.org/10.1159/000338506WOS000302752600021.pdf10.1159/000338506WOS:000302752600021The Th1/Th2 balance represents an important factor in the pathogenesis of renal ischemia-reperfusion injury (IRI). in addition, IRI causes a systemic inflammation that can affect other tissues, such as the lungs. To investigate the ability of renal IRI to modulate pulmonary function in a specific model of allergic inflammation, C57Bl/6 mice were immunized with ovalbumin/albumen on days 0 and 7 and challenged with an ovalbumin (OA) aerosol on days 14 and 21. After 24 h of the second antigen challenge, the animals were subjected to 45 minutes of ischemia. After 24 h of reperfusion, the bronchoalveolar lavage (BAL) fluid, blood and lung tissue were collected for analysis. Serum creatinine levels increased in both allergic and non-immunized animals subjected to IRI. However, BAL analysis showed a reduction in the total cells (46%) and neutrophils (58%) compared with control allergic animals not submitted to IRI. in addition, OA challenge induced the phosphorylation of ERK and Akt and the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in lung homogenates. After renal IRI, the phosphorylation of ERK and expression of COX-2 and iNOS were markedly reduced; however, there was no difference in the phosphorylation of Akt between sham and ischemic OA-challenged animals. Mucus production was also reduced in allergic mice after renal IRI. IL-4, IL-5 and IL-13 were markedly down-regulated in immunized/challenged mice subjected to IRI. These results suggest that renal IRI can modulate lung allergic inflammation, probably by altering the Th1/Th2 balance and, at least in part, by changing cellular signal transduction factors. Copyright (C) 2012 S. Karger AG, BaselConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Fundacao de Auxilio aos Docentes e Alunos-UNIFESP (FADA)Complex Fluids INCTFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Universidade Federal de São Paulo, Dept Ciencias Biol, Diadema, SP, BrazilUniv São Paulo, Fac Ciencias Farmaceut, Dept Anal Clin & Toxicol, São Paulo, BrazilUniversidade Federal de São Paulo, Disciplina Nefrol, Lab Imunol Clin & Expt, São Paulo, BrazilUniv São Paulo, Inst Ciencias Biomed, Dept Imunol, BR-05508 São Paulo, BrazilUniversidade Federal de São Paulo, Dept Ciencias Biol, Diadema, SP, BrazilUniversidade Federal de São Paulo, Disciplina Nefrol, Lab Imunol Clin & Expt, São Paulo, BrazilFAPESP: 07/07139-3FAPESP: 10/01404-0Web of Science523-532engKargerCellular Physiology and Biochemistryhttp://www.karger.com/Services/RightsPermissionsinfo:eu-repo/semantics/openAccessAsthmaRenal ischemia and reperfusionTh1/Th2 balanceLung allergic inflammationIRIModulation of Lung Allergic Response by Renal Ischemia and Reperfusion Injuryinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articlereponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESPORIGINALWOS000302752600021.pdfapplication/pdf563162${dspace.ui.url}/bitstream/11600/34385/1/WOS000302752600021.pdffe095798b12cc90c046698f9d0dd14bcMD51open accessTEXTWOS000302752600021.pdf.txtWOS000302752600021.pdf.txtExtracted texttext/plain40720${dspace.ui.url}/bitstream/11600/34385/9/WOS000302752600021.pdf.txt275973029a24ad0372ea49d73270aadcMD59open accessTHUMBNAILWOS000302752600021.pdf.jpgWOS000302752600021.pdf.jpgIM Thumbnailimage/jpeg6793${dspace.ui.url}/bitstream/11600/34385/11/WOS000302752600021.pdf.jpg7e36766cd224f3df7db217fad6987791MD511open access11600/343852023-06-05 19:24:25.326open accessoai:repositorio.unifesp.br:11600/34385Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestopendoar:34652023-06-05T22:24:25Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false
dc.title.en.fl_str_mv Modulation of Lung Allergic Response by Renal Ischemia and Reperfusion Injury
title Modulation of Lung Allergic Response by Renal Ischemia and Reperfusion Injury
spellingShingle Modulation of Lung Allergic Response by Renal Ischemia and Reperfusion Injury
Campanholle, Gabriela
Asthma
Renal ischemia and reperfusion
Th1/Th2 balance
Lung allergic inflammation
IRI
title_short Modulation of Lung Allergic Response by Renal Ischemia and Reperfusion Injury
title_full Modulation of Lung Allergic Response by Renal Ischemia and Reperfusion Injury
title_fullStr Modulation of Lung Allergic Response by Renal Ischemia and Reperfusion Injury
title_full_unstemmed Modulation of Lung Allergic Response by Renal Ischemia and Reperfusion Injury
title_sort Modulation of Lung Allergic Response by Renal Ischemia and Reperfusion Injury
author Campanholle, Gabriela
author_facet Campanholle, Gabriela
Silva, Reinaldo Correia [UNIFESP]
Martins, Joilson O.
Landgraf, Maristella A.
Paiva, Vanessa N.
Ferreira, Renaide Rodrigues [UNIFESP]
Amano, Mariane T.
Hiyane, Meire Ioshie [UNIFESP]
Cenedeze, Marcos Antonio [UNIFESP]
Pacheco-Silva, Alvaro [UNIFESP]
Camara, Niels Olsen Saraiva [UNIFESP]
Landgraf, Richardt Gama [UNIFESP]
author_role author
author2 Silva, Reinaldo Correia [UNIFESP]
Martins, Joilson O.
Landgraf, Maristella A.
Paiva, Vanessa N.
Ferreira, Renaide Rodrigues [UNIFESP]
Amano, Mariane T.
Hiyane, Meire Ioshie [UNIFESP]
Cenedeze, Marcos Antonio [UNIFESP]
Pacheco-Silva, Alvaro [UNIFESP]
Camara, Niels Olsen Saraiva [UNIFESP]
Landgraf, Richardt Gama [UNIFESP]
author2_role author
author
author
author
author
author
author
author
author
author
author
dc.contributor.institution.none.fl_str_mv Universidade Federal de São Paulo (UNIFESP)
Universidade de São Paulo (USP)
dc.contributor.author.fl_str_mv Campanholle, Gabriela
Silva, Reinaldo Correia [UNIFESP]
Martins, Joilson O.
Landgraf, Maristella A.
Paiva, Vanessa N.
Ferreira, Renaide Rodrigues [UNIFESP]
Amano, Mariane T.
Hiyane, Meire Ioshie [UNIFESP]
Cenedeze, Marcos Antonio [UNIFESP]
Pacheco-Silva, Alvaro [UNIFESP]
Camara, Niels Olsen Saraiva [UNIFESP]
Landgraf, Richardt Gama [UNIFESP]
dc.subject.eng.fl_str_mv Asthma
Renal ischemia and reperfusion
Th1/Th2 balance
Lung allergic inflammation
IRI
topic Asthma
Renal ischemia and reperfusion
Th1/Th2 balance
Lung allergic inflammation
IRI
description The Th1/Th2 balance represents an important factor in the pathogenesis of renal ischemia-reperfusion injury (IRI). in addition, IRI causes a systemic inflammation that can affect other tissues, such as the lungs. To investigate the ability of renal IRI to modulate pulmonary function in a specific model of allergic inflammation, C57Bl/6 mice were immunized with ovalbumin/albumen on days 0 and 7 and challenged with an ovalbumin (OA) aerosol on days 14 and 21. After 24 h of the second antigen challenge, the animals were subjected to 45 minutes of ischemia. After 24 h of reperfusion, the bronchoalveolar lavage (BAL) fluid, blood and lung tissue were collected for analysis. Serum creatinine levels increased in both allergic and non-immunized animals subjected to IRI. However, BAL analysis showed a reduction in the total cells (46%) and neutrophils (58%) compared with control allergic animals not submitted to IRI. in addition, OA challenge induced the phosphorylation of ERK and Akt and the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in lung homogenates. After renal IRI, the phosphorylation of ERK and expression of COX-2 and iNOS were markedly reduced; however, there was no difference in the phosphorylation of Akt between sham and ischemic OA-challenged animals. Mucus production was also reduced in allergic mice after renal IRI. IL-4, IL-5 and IL-13 were markedly down-regulated in immunized/challenged mice subjected to IRI. These results suggest that renal IRI can modulate lung allergic inflammation, probably by altering the Th1/Th2 balance and, at least in part, by changing cellular signal transduction factors. Copyright (C) 2012 S. Karger AG, Basel
publishDate 2012
dc.date.issued.fl_str_mv 2012-01-01
dc.date.accessioned.fl_str_mv 2016-01-24T14:17:38Z
dc.date.available.fl_str_mv 2016-01-24T14:17:38Z
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 Cellular Physiology and Biochemistry. Basel: Karger, v. 29, n. 3-4, p. 523-532, 2012.
dc.identifier.uri.fl_str_mv http://repositorio.unifesp.br/handle/11600/34385
http://dx.doi.org/10.1159/000338506
dc.identifier.issn.none.fl_str_mv 1015-8987
dc.identifier.file.none.fl_str_mv WOS000302752600021.pdf
dc.identifier.doi.none.fl_str_mv 10.1159/000338506
dc.identifier.wos.none.fl_str_mv WOS:000302752600021
identifier_str_mv Cellular Physiology and Biochemistry. Basel: Karger, v. 29, n. 3-4, p. 523-532, 2012.
1015-8987
WOS000302752600021.pdf
10.1159/000338506
WOS:000302752600021
url http://repositorio.unifesp.br/handle/11600/34385
http://dx.doi.org/10.1159/000338506
dc.language.iso.fl_str_mv eng
language eng
dc.relation.ispartof.none.fl_str_mv Cellular Physiology and Biochemistry
dc.rights.driver.fl_str_mv http://www.karger.com/Services/RightsPermissions
info:eu-repo/semantics/openAccess
rights_invalid_str_mv http://www.karger.com/Services/RightsPermissions
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 523-532
dc.publisher.none.fl_str_mv Karger
publisher.none.fl_str_mv Karger
dc.source.none.fl_str_mv reponame:Repositório Institucional da UNIFESP
instname:Universidade Federal de São Paulo (UNIFESP)
instacron:UNIFESP
instname_str Universidade Federal de São Paulo (UNIFESP)
instacron_str UNIFESP
institution UNIFESP
reponame_str Repositório Institucional da UNIFESP
collection Repositório Institucional da UNIFESP
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