Leukotrienes Produced in Allergic Lung Inflammation Activate Alveolar Macrophages

Detalhes bibliográficos
Autor(a) principal: Silva, Reinaldo Correia [UNIFESP]
Data de Publicação: 2010
Outros Autores: Landgraf, Maristella de Almeida, Hiyane, Meire Ioshie [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/11600/32040
http://dx.doi.org/10.1159/000320555
Resumo: It has been well-documented that leukotrienes (LTs) are released in allergic lung inflammation and that they participate in the physiopathology of asthma. A role for LTs in innate immunity has recently emerged: Cys-LTs were shown to enhance Fc gamma R-mediated phagocytosis by alveolar macrophages (AMs). Thus, using a rat model of asthma, we evaluated Fc gamma R-mediated phagocytosis and killing of Klebsiella pneumoniae by AMs. the effect of treatment with a cys-LT antagonist (montelukast) on macrophage function was also investigated. Male Wistar rats were immunized twice with OVA/alumen intraperitoneally and challenged with OVA aerosol. After 24 h, the animals were killed, and the AMs were obtained by bronchoalveolar lavage. Macrophages were cultured with IgG-opsonized red blood cells (50: 1) or IgG-opsonized K. pneumoniae (30: 1), and phagocytosis or killing was evaluated. Leukotriene C(4) and nitric oxide were quantified by the EIA and Griess methods, respectively. the results showed that AMs from sensitized and challenged rats presented a markedly increased phagocytic capacity via Fc gamma R (10X compared to controls) and enhanced killing of K. pneumoniae (4X higher than controls). the increased phagocytosis was inhibited 15X and killing 3X by treatment of the rats with montelukast, as compared to the non-treated group. cys-LT addition increased phagocytosis in control AMs but had no effect on macrophages from allergic lungs. Montelukast reduced nitric oxide (39%) and LTC(4) (73%). These results suggest that LTs produced during allergic lung inflammation potentiate the capacity of AMs to phagocytose and kill K. pneumonia via Fc gamma R. Copyright (C) 2010 S. Karger AG, Basel
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spelling Silva, Reinaldo Correia [UNIFESP]Landgraf, Maristella de AlmeidaHiyane, Meire Ioshie [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)2016-01-24T13:59:01Z2016-01-24T13:59:01Z2010-01-01Cellular Physiology and Biochemistry. Basel: Karger, v. 26, n. 3, p. 319-326, 2010.1015-8987http://repositorio.unifesp.br/handle/11600/32040http://dx.doi.org/10.1159/000320555WOS000281236600007.pdf10.1159/000320555WOS:000281236600007It has been well-documented that leukotrienes (LTs) are released in allergic lung inflammation and that they participate in the physiopathology of asthma. A role for LTs in innate immunity has recently emerged: Cys-LTs were shown to enhance Fc gamma R-mediated phagocytosis by alveolar macrophages (AMs). Thus, using a rat model of asthma, we evaluated Fc gamma R-mediated phagocytosis and killing of Klebsiella pneumoniae by AMs. the effect of treatment with a cys-LT antagonist (montelukast) on macrophage function was also investigated. Male Wistar rats were immunized twice with OVA/alumen intraperitoneally and challenged with OVA aerosol. After 24 h, the animals were killed, and the AMs were obtained by bronchoalveolar lavage. Macrophages were cultured with IgG-opsonized red blood cells (50: 1) or IgG-opsonized K. pneumoniae (30: 1), and phagocytosis or killing was evaluated. Leukotriene C(4) and nitric oxide were quantified by the EIA and Griess methods, respectively. the results showed that AMs from sensitized and challenged rats presented a markedly increased phagocytic capacity via Fc gamma R (10X compared to controls) and enhanced killing of K. pneumoniae (4X higher than controls). the increased phagocytosis was inhibited 15X and killing 3X by treatment of the rats with montelukast, as compared to the non-treated group. cys-LT addition increased phagocytosis in control AMs but had no effect on macrophages from allergic lungs. Montelukast reduced nitric oxide (39%) and LTC(4) (73%). These results suggest that LTs produced during allergic lung inflammation potentiate the capacity of AMs to phagocytose and kill K. pneumonia via Fc gamma R. Copyright (C) 2010 S. Karger AG, BaselConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Complex Fluids INCTFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Universidade Federal de São Paulo, Disciplina Nefrol, Dept Nefrol, Lab Imunol Clin & Expt, BR-04023900 São Paulo, BrazilUniv São Paulo, Dept Imunol, Lab Imunol Transplantes, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Ciencias Biol, BR-04023900 São Paulo, BrazilUniversidade Federal de São Paulo, Disciplina Nefrol, Dept Nefrol, Lab Imunol Clin & Expt, BR-04023900 São Paulo, BrazilUniversidade Federal de São Paulo, Dept Ciencias Biol, BR-04023900 São Paulo, BrazilFAPESP: 07/07139-3FAPESP: 09/52119-6FAPESP: 10/01404-0Web of Science319-326engKargerCellular Physiology and Biochemistryhttp://www.karger.com/Services/RightsPermissionsinfo:eu-repo/semantics/openAccessAlveolar macrophagesLeukotrienesAsthmaKillingKlebsiella pneumoniaeLeukotrienes Produced in Allergic Lung Inflammation Activate Alveolar Macrophagesinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articlereponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESPORIGINALWOS000281236600007.pdfapplication/pdf374377${dspace.ui.url}/bitstream/11600/32040/1/WOS000281236600007.pdff4aeeb81b36340f809e7566f00531968MD51open accessTEXTWOS000281236600007.pdf.txtWOS000281236600007.pdf.txtExtracted texttext/plain34481${dspace.ui.url}/bitstream/11600/32040/2/WOS000281236600007.pdf.txt07c140d05e8310bdf2cdf655cc190e8aMD52open access11600/320402022-11-04 15:40:33.419open accessoai:repositorio.unifesp.br:11600/32040Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestopendoar:34652022-11-04T18:40:33Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false
dc.title.en.fl_str_mv Leukotrienes Produced in Allergic Lung Inflammation Activate Alveolar Macrophages
title Leukotrienes Produced in Allergic Lung Inflammation Activate Alveolar Macrophages
spellingShingle Leukotrienes Produced in Allergic Lung Inflammation Activate Alveolar Macrophages
Silva, Reinaldo Correia [UNIFESP]
Alveolar macrophages
Leukotrienes
Asthma
Killing
Klebsiella pneumoniae
title_short Leukotrienes Produced in Allergic Lung Inflammation Activate Alveolar Macrophages
title_full Leukotrienes Produced in Allergic Lung Inflammation Activate Alveolar Macrophages
title_fullStr Leukotrienes Produced in Allergic Lung Inflammation Activate Alveolar Macrophages
title_full_unstemmed Leukotrienes Produced in Allergic Lung Inflammation Activate Alveolar Macrophages
title_sort Leukotrienes Produced in Allergic Lung Inflammation Activate Alveolar Macrophages
author Silva, Reinaldo Correia [UNIFESP]
author_facet Silva, Reinaldo Correia [UNIFESP]
Landgraf, Maristella de Almeida
Hiyane, Meire Ioshie [UNIFESP]
Pacheco-Silva, Alvaro [UNIFESP]
Camara, Niels Olsen Saraiva [UNIFESP]
Landgraf, Richardt Gama [UNIFESP]
author_role author
author2 Landgraf, Maristella de Almeida
Hiyane, Meire Ioshie [UNIFESP]
Pacheco-Silva, Alvaro [UNIFESP]
Camara, Niels Olsen Saraiva [UNIFESP]
Landgraf, Richardt Gama [UNIFESP]
author2_role 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 Silva, Reinaldo Correia [UNIFESP]
Landgraf, Maristella de Almeida
Hiyane, Meire Ioshie [UNIFESP]
Pacheco-Silva, Alvaro [UNIFESP]
Camara, Niels Olsen Saraiva [UNIFESP]
Landgraf, Richardt Gama [UNIFESP]
dc.subject.eng.fl_str_mv Alveolar macrophages
Leukotrienes
Asthma
Killing
Klebsiella pneumoniae
topic Alveolar macrophages
Leukotrienes
Asthma
Killing
Klebsiella pneumoniae
description It has been well-documented that leukotrienes (LTs) are released in allergic lung inflammation and that they participate in the physiopathology of asthma. A role for LTs in innate immunity has recently emerged: Cys-LTs were shown to enhance Fc gamma R-mediated phagocytosis by alveolar macrophages (AMs). Thus, using a rat model of asthma, we evaluated Fc gamma R-mediated phagocytosis and killing of Klebsiella pneumoniae by AMs. the effect of treatment with a cys-LT antagonist (montelukast) on macrophage function was also investigated. Male Wistar rats were immunized twice with OVA/alumen intraperitoneally and challenged with OVA aerosol. After 24 h, the animals were killed, and the AMs were obtained by bronchoalveolar lavage. Macrophages were cultured with IgG-opsonized red blood cells (50: 1) or IgG-opsonized K. pneumoniae (30: 1), and phagocytosis or killing was evaluated. Leukotriene C(4) and nitric oxide were quantified by the EIA and Griess methods, respectively. the results showed that AMs from sensitized and challenged rats presented a markedly increased phagocytic capacity via Fc gamma R (10X compared to controls) and enhanced killing of K. pneumoniae (4X higher than controls). the increased phagocytosis was inhibited 15X and killing 3X by treatment of the rats with montelukast, as compared to the non-treated group. cys-LT addition increased phagocytosis in control AMs but had no effect on macrophages from allergic lungs. Montelukast reduced nitric oxide (39%) and LTC(4) (73%). These results suggest that LTs produced during allergic lung inflammation potentiate the capacity of AMs to phagocytose and kill K. pneumonia via Fc gamma R. Copyright (C) 2010 S. Karger AG, Basel
publishDate 2010
dc.date.issued.fl_str_mv 2010-01-01
dc.date.accessioned.fl_str_mv 2016-01-24T13:59:01Z
dc.date.available.fl_str_mv 2016-01-24T13:59:01Z
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.citation.fl_str_mv Cellular Physiology and Biochemistry. Basel: Karger, v. 26, n. 3, p. 319-326, 2010.
dc.identifier.uri.fl_str_mv http://repositorio.unifesp.br/handle/11600/32040
http://dx.doi.org/10.1159/000320555
dc.identifier.issn.none.fl_str_mv 1015-8987
dc.identifier.file.none.fl_str_mv WOS000281236600007.pdf
dc.identifier.doi.none.fl_str_mv 10.1159/000320555
dc.identifier.wos.none.fl_str_mv WOS:000281236600007
identifier_str_mv Cellular Physiology and Biochemistry. Basel: Karger, v. 26, n. 3, p. 319-326, 2010.
1015-8987
WOS000281236600007.pdf
10.1159/000320555
WOS:000281236600007
url http://repositorio.unifesp.br/handle/11600/32040
http://dx.doi.org/10.1159/000320555
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 319-326
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
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