Leukotrienes Produced in Allergic Lung Inflammation Activate Alveolar Macrophages
Autor(a) principal: | |
---|---|
Data de Publicação: | 2010 |
Outros Autores: | , , , , |
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 |
id |
UFSP_054c92f48dd4d1f4747a2a5d421cbb1d |
---|---|
oai_identifier_str |
oai:repositorio.unifesp.br:11600/32040 |
network_acronym_str |
UFSP |
network_name_str |
Repositório Institucional da UNIFESP |
repository_id_str |
3465 |
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 |
collection |
Repositório Institucional da UNIFESP |
bitstream.url.fl_str_mv |
${dspace.ui.url}/bitstream/11600/32040/1/WOS000281236600007.pdf ${dspace.ui.url}/bitstream/11600/32040/2/WOS000281236600007.pdf.txt |
bitstream.checksum.fl_str_mv |
f4aeeb81b36340f809e7566f00531968 07c140d05e8310bdf2cdf655cc190e8a |
bitstream.checksumAlgorithm.fl_str_mv |
MD5 MD5 |
repository.name.fl_str_mv |
Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP) |
repository.mail.fl_str_mv |
|
_version_ |
1802764187694268416 |