Regulation of eosinophilia and allergic airway inflammation by the glycan-binding protein galectin-1

Galectin-1 (Gal-1), a glycan-binding protein with broad antiinflammatory activities, functions as a proresolving mediator in autoimmune and chronic inflammatory disorders. However, its role in allergic airway inflammation has not yet been elucidated. We evaluated the effects of Gal-1 on eosinophil f...

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Publicado:	2016
Materias:	Allergic airway inflammation Apoptosis Eosinophils Galectin-1 Migration allergen alpha4 integrin CD11b antigen CD18 antigen cell surface receptor chemokine receptor CCR3 cytoskeleton protein eotaxin eotaxin 2 F actin galectin 1 glycan interleukin 13 interleukin 5 L selectin lymphocyte function associated antigen 1 mitogen activated protein kinase 1 mitogen activated protein kinase 3 transforming growth factor beta tumor necrosis factor alpha vascular cell adhesion molecule 1 chemokine cytokine allergic asthma animal cell animal experiment animal model animal tissue apoptosis Article bone marrow cell CD3+ T lymphocyte cell adhesion comparative study concentration response controlled study cytoskeleton enzyme activation eosinophil eosinophilia extracellular space immunoregulation in vitro study in vivo study inflammatory cell leukocyte function leukocyte migration lung migration inhibition mouse nonhuman priority journal protein expression protein function protein localization protein protein interaction animal asthma C57BL mouse chemistry physiology Animals Asthma Cell Adhesion Chemokines Cytokines Eosinophilia Galectin 1 Lung Mice Mice, Inbred C57BL
Acceso en línea:	https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00278424_v113_n33_pE4837_Ge http://hdl.handle.net/20.500.12110/paper_00278424_v113_n33_pE4837_Ge
Aporte de:	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) de Universidad de Buenos Aires

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spelling	paper:paper_00278424_v113_n33_pE4837_Ge2023-06-08T14:54:31Z Regulation of eosinophilia and allergic airway inflammation by the glycan-binding protein galectin-1 Allergic airway inflammation Apoptosis Eosinophils Galectin-1 Migration allergen alpha4 integrin CD11b antigen CD18 antigen cell surface receptor chemokine receptor CCR3 cytoskeleton protein eotaxin eotaxin 2 F actin galectin 1 glycan interleukin 13 interleukin 5 L selectin lymphocyte function associated antigen 1 mitogen activated protein kinase 1 mitogen activated protein kinase 3 transforming growth factor beta tumor necrosis factor alpha vascular cell adhesion molecule 1 chemokine cytokine galectin 1 allergic asthma animal cell animal experiment animal model animal tissue apoptosis Article bone marrow cell CD3+ T lymphocyte cell adhesion comparative study concentration response controlled study cytoskeleton enzyme activation eosinophil eosinophilia extracellular space immunoregulation in vitro study in vivo study inflammatory cell leukocyte function leukocyte migration lung migration inhibition mouse nonhuman priority journal protein expression protein function protein localization protein protein interaction animal asthma C57BL mouse chemistry eosinophilia physiology Animals Apoptosis Asthma Cell Adhesion Chemokines Cytokines Eosinophilia Eosinophils Galectin 1 Lung Mice Mice, Inbred C57BL Galectin-1 (Gal-1), a glycan-binding protein with broad antiinflammatory activities, functions as a proresolving mediator in autoimmune and chronic inflammatory disorders. However, its role in allergic airway inflammation has not yet been elucidated. We evaluated the effects of Gal-1 on eosinophil function and its role in a mouse model of allergic asthma. Allergen exposure resulted in airway recruitment of Gal-1-expressing inflammatory cells, including eosinophils, as well as increased Gal-1 in extracellular spaces in the lungs. In vitro, extracellular Gal-1 exerted divergent effects on eosinophils that were N-glycan- And dose-dependent. At concentrations ≤0.25 μM, Gal-1 increased eosinophil adhesion to vascular cell adhesion molecule-1, caused redistribution of integrin CD49d to the periphery and cell clustering, but inhibited ERK(1/2) activation and eotaxin-1-induced migration. Exposure to concentrations ≥1 μM resulted in ERK(1/2)- dependent apoptosis and disruption of the F- Actin cytoskeleton. At lower concentrations, Gal-1 did not alter expression of adhesion molecules (CD49d, CD18, CD11a, CD11b, L-selectin) or of the chemokine receptor CCR3, but decreased CD49d and CCR3 was observed in eosinophils treated with higher concentrations of this lectin. In vivo, allergen-challenged Gal-1-deficient mice exhibited increased recruitment of eosinophils and CD3+ T lymphocytes in the airways as well as elevated peripheral blood and bone marrow eosinophils relative to corresponding WT mice. Further, these mice had an increased propensity to develop airway hyperresponsiveness and displayed significantly elevated levels of TNF-α in lung tissue. This study suggests that Gal-1 can limit eosinophil recruitment to allergic airways and suppresses airway inflammation by inhibiting cell migration and promoting eosinophil apoptosis. 2016 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00278424_v113_n33_pE4837_Ge http://hdl.handle.net/20.500.12110/paper_00278424_v113_n33_pE4837_Ge
institution	Universidad de Buenos Aires
institution_str	I-28
repository_str	R-134
collection	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic	Allergic airway inflammation Apoptosis Eosinophils Galectin-1 Migration allergen alpha4 integrin CD11b antigen CD18 antigen cell surface receptor chemokine receptor CCR3 cytoskeleton protein eotaxin eotaxin 2 F actin galectin 1 glycan interleukin 13 interleukin 5 L selectin lymphocyte function associated antigen 1 mitogen activated protein kinase 1 mitogen activated protein kinase 3 transforming growth factor beta tumor necrosis factor alpha vascular cell adhesion molecule 1 chemokine cytokine galectin 1 allergic asthma animal cell animal experiment animal model animal tissue apoptosis Article bone marrow cell CD3+ T lymphocyte cell adhesion comparative study concentration response controlled study cytoskeleton enzyme activation eosinophil eosinophilia extracellular space immunoregulation in vitro study in vivo study inflammatory cell leukocyte function leukocyte migration lung migration inhibition mouse nonhuman priority journal protein expression protein function protein localization protein protein interaction animal asthma C57BL mouse chemistry eosinophilia physiology Animals Apoptosis Asthma Cell Adhesion Chemokines Cytokines Eosinophilia Eosinophils Galectin 1 Lung Mice Mice, Inbred C57BL
spellingShingle	Allergic airway inflammation Apoptosis Eosinophils Galectin-1 Migration allergen alpha4 integrin CD11b antigen CD18 antigen cell surface receptor chemokine receptor CCR3 cytoskeleton protein eotaxin eotaxin 2 F actin galectin 1 glycan interleukin 13 interleukin 5 L selectin lymphocyte function associated antigen 1 mitogen activated protein kinase 1 mitogen activated protein kinase 3 transforming growth factor beta tumor necrosis factor alpha vascular cell adhesion molecule 1 chemokine cytokine galectin 1 allergic asthma animal cell animal experiment animal model animal tissue apoptosis Article bone marrow cell CD3+ T lymphocyte cell adhesion comparative study concentration response controlled study cytoskeleton enzyme activation eosinophil eosinophilia extracellular space immunoregulation in vitro study in vivo study inflammatory cell leukocyte function leukocyte migration lung migration inhibition mouse nonhuman priority journal protein expression protein function protein localization protein protein interaction animal asthma C57BL mouse chemistry eosinophilia physiology Animals Apoptosis Asthma Cell Adhesion Chemokines Cytokines Eosinophilia Eosinophils Galectin 1 Lung Mice Mice, Inbred C57BL Regulation of eosinophilia and allergic airway inflammation by the glycan-binding protein galectin-1
topic_facet	Allergic airway inflammation Apoptosis Eosinophils Galectin-1 Migration allergen alpha4 integrin CD11b antigen CD18 antigen cell surface receptor chemokine receptor CCR3 cytoskeleton protein eotaxin eotaxin 2 F actin galectin 1 glycan interleukin 13 interleukin 5 L selectin lymphocyte function associated antigen 1 mitogen activated protein kinase 1 mitogen activated protein kinase 3 transforming growth factor beta tumor necrosis factor alpha vascular cell adhesion molecule 1 chemokine cytokine galectin 1 allergic asthma animal cell animal experiment animal model animal tissue apoptosis Article bone marrow cell CD3+ T lymphocyte cell adhesion comparative study concentration response controlled study cytoskeleton enzyme activation eosinophil eosinophilia extracellular space immunoregulation in vitro study in vivo study inflammatory cell leukocyte function leukocyte migration lung migration inhibition mouse nonhuman priority journal protein expression protein function protein localization protein protein interaction animal asthma C57BL mouse chemistry eosinophilia physiology Animals Apoptosis Asthma Cell Adhesion Chemokines Cytokines Eosinophilia Eosinophils Galectin 1 Lung Mice Mice, Inbred C57BL
description	Galectin-1 (Gal-1), a glycan-binding protein with broad antiinflammatory activities, functions as a proresolving mediator in autoimmune and chronic inflammatory disorders. However, its role in allergic airway inflammation has not yet been elucidated. We evaluated the effects of Gal-1 on eosinophil function and its role in a mouse model of allergic asthma. Allergen exposure resulted in airway recruitment of Gal-1-expressing inflammatory cells, including eosinophils, as well as increased Gal-1 in extracellular spaces in the lungs. In vitro, extracellular Gal-1 exerted divergent effects on eosinophils that were N-glycan- And dose-dependent. At concentrations ≤0.25 μM, Gal-1 increased eosinophil adhesion to vascular cell adhesion molecule-1, caused redistribution of integrin CD49d to the periphery and cell clustering, but inhibited ERK(1/2) activation and eotaxin-1-induced migration. Exposure to concentrations ≥1 μM resulted in ERK(1/2)- dependent apoptosis and disruption of the F- Actin cytoskeleton. At lower concentrations, Gal-1 did not alter expression of adhesion molecules (CD49d, CD18, CD11a, CD11b, L-selectin) or of the chemokine receptor CCR3, but decreased CD49d and CCR3 was observed in eosinophils treated with higher concentrations of this lectin. In vivo, allergen-challenged Gal-1-deficient mice exhibited increased recruitment of eosinophils and CD3+ T lymphocytes in the airways as well as elevated peripheral blood and bone marrow eosinophils relative to corresponding WT mice. Further, these mice had an increased propensity to develop airway hyperresponsiveness and displayed significantly elevated levels of TNF-α in lung tissue. This study suggests that Gal-1 can limit eosinophil recruitment to allergic airways and suppresses airway inflammation by inhibiting cell migration and promoting eosinophil apoptosis.
title	Regulation of eosinophilia and allergic airway inflammation by the glycan-binding protein galectin-1
title_short	Regulation of eosinophilia and allergic airway inflammation by the glycan-binding protein galectin-1
title_full	Regulation of eosinophilia and allergic airway inflammation by the glycan-binding protein galectin-1
title_fullStr	Regulation of eosinophilia and allergic airway inflammation by the glycan-binding protein galectin-1
title_full_unstemmed	Regulation of eosinophilia and allergic airway inflammation by the glycan-binding protein galectin-1
title_sort	regulation of eosinophilia and allergic airway inflammation by the glycan-binding protein galectin-1
publishDate	2016
url	https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00278424_v113_n33_pE4837_Ge http://hdl.handle.net/20.500.12110/paper_00278424_v113_n33_pE4837_Ge
_version_	1768545498400030720

Regulation of eosinophilia and allergic airway inflammation by the glycan-binding protein galectin-1

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