Eosinophil recruitment to the lung in a murine model of allergic inflammation : the role of T Cells, chemokines, and adhesion receptors

Eosinophil accumulation is a distinctive feature of lung allergic inflammation. Here, we have used a mouse model of OVA (ovalbumin)-induced pulmonary eosinophilia to study the cellular and molecular mechanisms for this selective recruitment of eosinophils to the airways. In this model there was an e...

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Detalhes bibliográficos
Autores: Gonzalo, José Ángel, Lloyd, Clare M., Kremer, Leonor, Finger, Elizabeth, Martínez-Alonso, Carlos, Siegelman, M.H., Cybulsky, Myron, Gutiérrez Ramos, José Carlos
Formato: artículo
Fecha de publicación:1996
País:España
Recursos:Consejo Superior de Investigaciones Científicas (CSIC)
Repositorio:DIGITAL.CSIC. Repositorio Institucional del CSIC
OAI Identifier:oai:digital.csic.es:10261/3617
Acesso em linha:http://hdl.handle.net/10261/3617
Access Level:acceso abierto
Palavra-chave:Lung eosinophilia
Leukocytes
Chemotactic cytokines
Integrins
Selectins
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spelling Eosinophil recruitment to the lung in a murine model of allergic inflammation : the role of T Cells, chemokines, and adhesion receptorsGonzalo, José ÁngelLloyd, Clare M.Kremer, LeonorFinger, ElizabethMartínez-Alonso, CarlosSiegelman, M.H.Cybulsky, MyronGutiérrez Ramos, José CarlosLung eosinophiliaLeukocytesChemotactic cytokinesIntegrinsSelectinsEosinophil accumulation is a distinctive feature of lung allergic inflammation. Here, we have used a mouse model of OVA (ovalbumin)-induced pulmonary eosinophilia to study the cellular and molecular mechanisms for this selective recruitment of eosinophils to the airways. In this model there was an early accumulation of infiltrating monocytes/macrophages in the lung during the OVA treatment, whereas the increase in infiltrating T-lymphocytes paralleled the accumulation of eosinophils. The kinetics of accumulation of these three leukocyte subtypes correlated with the levels of mRNA expression of the chemokines monocyte chemotactic peptide-1/JE, eotaxin, and RANTES (regulated upon activation in normal T cells expressed and secreted), suggesting their involvement in the recruitment of these leukocytes. Furthermore, blockade of eotaxin with specific antibodies in vivo reduced the accumulation of eosinophils in the lung in response to OVA by half. Mature CD4 1 T-lymphocytes were absolutely required for OVA-induced eosinophil accumulation since lung eosinophilia was prevented in CD4 1 -deficient mice. However, these cells were neither the main producers of the major eosinophilic chemokines eotaxin, RANTES, or MIP-1 a, nor did they regulate the expression of these chemokines. Rather, the presence of CD4 1 T cells was necessary for enhancement of VCAM-1 (vascular cell adhesion molecule-1) expression in the lung during allergic inflammation induced by the OVA treatment. In support of this, mice genetically deficient for VCAM-1 and intercellular adhesion molecule-1 failed to develop pulmonary eosinophilia. Selective eosinophilic recruitment during lung allergic inflammation results from a sequential accumulation of certain leukocyte types, particularly T cells, and relies on the presence of both eosinophilic chemoattractants and adhesion receptors.Peer reviewedAmerican Society for Clinical Investigation200820081996info:eu-repo/semantics/articlehttp://purl.org/coar/resource_type/c_650126512709 bytesapplication/pdfhttp://hdl.handle.net/10261/3617reponame:DIGITAL.CSIC. Repositorio Institucional del CSICinstname:Consejo Superior de Investigaciones Científicas (CSIC)Inglésinfo:eu-repo/semantics/openAccessoai:digital.csic.es:10261/36172026-05-22T06:33:51Z
dc.title.none.fl_str_mv Eosinophil recruitment to the lung in a murine model of allergic inflammation : the role of T Cells, chemokines, and adhesion receptors
title Eosinophil recruitment to the lung in a murine model of allergic inflammation : the role of T Cells, chemokines, and adhesion receptors
spellingShingle Eosinophil recruitment to the lung in a murine model of allergic inflammation : the role of T Cells, chemokines, and adhesion receptors
Gonzalo, José Ángel
Lung eosinophilia
Leukocytes
Chemotactic cytokines
Integrins
Selectins
title_short Eosinophil recruitment to the lung in a murine model of allergic inflammation : the role of T Cells, chemokines, and adhesion receptors
title_full Eosinophil recruitment to the lung in a murine model of allergic inflammation : the role of T Cells, chemokines, and adhesion receptors
title_fullStr Eosinophil recruitment to the lung in a murine model of allergic inflammation : the role of T Cells, chemokines, and adhesion receptors
title_full_unstemmed Eosinophil recruitment to the lung in a murine model of allergic inflammation : the role of T Cells, chemokines, and adhesion receptors
title_sort Eosinophil recruitment to the lung in a murine model of allergic inflammation : the role of T Cells, chemokines, and adhesion receptors
dc.creator.none.fl_str_mv Gonzalo, José Ángel
Lloyd, Clare M.
Kremer, Leonor
Finger, Elizabeth
Martínez-Alonso, Carlos
Siegelman, M.H.
Cybulsky, Myron
Gutiérrez Ramos, José Carlos
author Gonzalo, José Ángel
author_facet Gonzalo, José Ángel
Lloyd, Clare M.
Kremer, Leonor
Finger, Elizabeth
Martínez-Alonso, Carlos
Siegelman, M.H.
Cybulsky, Myron
Gutiérrez Ramos, José Carlos
author_role author
author2 Lloyd, Clare M.
Kremer, Leonor
Finger, Elizabeth
Martínez-Alonso, Carlos
Siegelman, M.H.
Cybulsky, Myron
Gutiérrez Ramos, José Carlos
author2_role author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Lung eosinophilia
Leukocytes
Chemotactic cytokines
Integrins
Selectins
topic Lung eosinophilia
Leukocytes
Chemotactic cytokines
Integrins
Selectins
description Eosinophil accumulation is a distinctive feature of lung allergic inflammation. Here, we have used a mouse model of OVA (ovalbumin)-induced pulmonary eosinophilia to study the cellular and molecular mechanisms for this selective recruitment of eosinophils to the airways. In this model there was an early accumulation of infiltrating monocytes/macrophages in the lung during the OVA treatment, whereas the increase in infiltrating T-lymphocytes paralleled the accumulation of eosinophils. The kinetics of accumulation of these three leukocyte subtypes correlated with the levels of mRNA expression of the chemokines monocyte chemotactic peptide-1/JE, eotaxin, and RANTES (regulated upon activation in normal T cells expressed and secreted), suggesting their involvement in the recruitment of these leukocytes. Furthermore, blockade of eotaxin with specific antibodies in vivo reduced the accumulation of eosinophils in the lung in response to OVA by half. Mature CD4 1 T-lymphocytes were absolutely required for OVA-induced eosinophil accumulation since lung eosinophilia was prevented in CD4 1 -deficient mice. However, these cells were neither the main producers of the major eosinophilic chemokines eotaxin, RANTES, or MIP-1 a, nor did they regulate the expression of these chemokines. Rather, the presence of CD4 1 T cells was necessary for enhancement of VCAM-1 (vascular cell adhesion molecule-1) expression in the lung during allergic inflammation induced by the OVA treatment. In support of this, mice genetically deficient for VCAM-1 and intercellular adhesion molecule-1 failed to develop pulmonary eosinophilia. Selective eosinophilic recruitment during lung allergic inflammation results from a sequential accumulation of certain leukocyte types, particularly T cells, and relies on the presence of both eosinophilic chemoattractants and adhesion receptors.
publishDate 1996
dc.date.none.fl_str_mv 1996
2008
2008
dc.type.none.fl_str_mv info:eu-repo/semantics/article
http://purl.org/coar/resource_type/c_6501
format article
dc.identifier.none.fl_str_mv http://hdl.handle.net/10261/3617
url http://hdl.handle.net/10261/3617
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 26512709 bytes
application/pdf
dc.publisher.none.fl_str_mv American Society for Clinical Investigation
publisher.none.fl_str_mv American Society for Clinical Investigation
dc.source.none.fl_str_mv reponame:DIGITAL.CSIC. Repositorio Institucional del CSIC
instname:Consejo Superior de Investigaciones Científicas (CSIC)
instname_str Consejo Superior de Investigaciones Científicas (CSIC)
reponame_str DIGITAL.CSIC. Repositorio Institucional del CSIC
collection DIGITAL.CSIC. Repositorio Institucional del CSIC
repository.name.fl_str_mv
repository.mail.fl_str_mv
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