Tumor necrosis factor-related apoptosis-inducing ligand mediates the resolution of allergic airway inflammation induced by chronic allergen inhalation

Allergic asthma can vanish over time either spontaneously or induced by allergen-specific immunotherapy. In mice with established airway allergic inflammation, chronic intranasal (IN) allergen challenges decreases progressively airway allergic inflammation. Here we compared the contribution of diffe...

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Veröffentlicht in:Mucosal immunology 2014-09, Vol.7 (5), p.1199-1208
Hauptverfasser: Faustino, L, Fonseca, D M, Florsheim, E B, Resende, R R, Lepique, A P, Faquim-Mauro, E, Gomes, E, Silva, J S, Yagita, H, Russo, M
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container_title Mucosal immunology
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creator Faustino, L
Fonseca, D M
Florsheim, E B
Resende, R R
Lepique, A P
Faquim-Mauro, E
Gomes, E
Silva, J S
Yagita, H
Russo, M
description Allergic asthma can vanish over time either spontaneously or induced by allergen-specific immunotherapy. In mice with established airway allergic inflammation, chronic intranasal (IN) allergen challenges decreases progressively airway allergic inflammation. Here we compared the contribution of different regulatory pathways that could be associated with this phenomenon, known as local inhalational tolerance. We found that inhalational tolerance was not associated with increased number of regulatory T cells or suppressive cytokines. Instead, it was associated with increased apoptosis of airway inflammatory leukocytes revealed by annexin-V staining and the expression of apical caspase 8 and effector caspase 3. Also, the transition from acute to chronic phase was associated with a shift in the expression of pro-allergic to pro-apoptotic molecules. The tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) was found to be a key molecule in mediating resolution of allergic inflammation because anti-TRAIL treatment blocked apoptosis and increased the infiltration of T helper type 2 (Th2) cells and eosinophils. Notably, repeated IN treatment with recombinant TRAIL in established airway allergic inflammation augmented leukocyte apoptosis and decreased the frequency of interleukin-5-producing Th2 cells and eosinophils to airways. Our data indicate that TRAIL signaling is sufficient for downmodulation of allergic airway disease, suggesting a potential therapeutic use of TRAIL for asthma treatment.
doi_str_mv 10.1038/mi.2014.9
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The tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) was found to be a key molecule in mediating resolution of allergic inflammation because anti-TRAIL treatment blocked apoptosis and increased the infiltration of T helper type 2 (Th2) cells and eosinophils. Notably, repeated IN treatment with recombinant TRAIL in established airway allergic inflammation augmented leukocyte apoptosis and decreased the frequency of interleukin-5-producing Th2 cells and eosinophils to airways. 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subjects 631/250/249/2510/31
631/250/249/2510/9
631/250/347
631/80/86
Allergens - immunology
Allergology
Animals
Antibodies
Antibodies, Monoclonal - immunology
Apoptosis - immunology
Biomedical and Life Sciences
Biomedicine
Caspase 3 - genetics
Caspase 3 - metabolism
Caspase 8 - genetics
Caspase 8 - metabolism
Chronic Disease
Female
Gastroenterology
Gene Expression Regulation - immunology
Immunology
Inflammation - drug therapy
Inflammation - immunology
Lung - immunology
Lung - physiopathology
Mice
Mice, Knockout
Recombinant Proteins - genetics
Respiratory Hypersensitivity - drug therapy
Respiratory Hypersensitivity - immunology
Th2 Cells - immunology
TNF-Related Apoptosis-Inducing Ligand - genetics
TNF-Related Apoptosis-Inducing Ligand - metabolism
TNF-Related Apoptosis-Inducing Ligand - therapeutic use
title Tumor necrosis factor-related apoptosis-inducing ligand mediates the resolution of allergic airway inflammation induced by chronic allergen inhalation
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