Increased IL-6 and Potential IL-6 ...
Type de document :
Article dans une revue scientifique
DOI :
PMID :
URL permanente :
Titre :
Increased IL-6 and Potential IL-6 trans-signalling in the airways after an allergen challenge.
Auteur(s) :
Esnault, Stephane [Auteur]
Khosravi, Mehdi [Auteur]
Kelly, Elizabeth A [Auteur]
Liu, Lin Ying [Auteur]
Bochkov, Yury A [Auteur]
Tattersall, Matthew C [Auteur]
Jarjour, Nizar N [Auteur]
Khosravi, Mehdi [Auteur]
Kelly, Elizabeth A [Auteur]
Liu, Lin Ying [Auteur]
Bochkov, Yury A [Auteur]
Tattersall, Matthew C [Auteur]
Jarjour, Nizar N [Auteur]
Titre de la revue :
Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology
Nom court de la revue :
Clin Exp Allergy
Numéro :
51
Pagination :
564-573
Date de publication :
2021-04-01
ISSN :
1365-2222
Mot(s)-clé(s) en anglais :
Allergens
Ambrosia
Animals
Asthma
Bronchial Provocation Tests
Bronchoalveolar Lavage Fluid
Chemokine CCL2
Cytokine Receptor gp130
Dander
Female
Humans
Interleukin-6
Male
Pyroglyphidae
RNA-Seq
Receptors, Interleukin-6
Respiratory Hypersensitivity
Young Adult
CCL2
IL-6
IL-6 receptor
allergy
asthma
bronchoalveolar lavage
fibroblasts
trans-signalling
Ambrosia
Animals
Asthma
Bronchial Provocation Tests
Bronchoalveolar Lavage Fluid
Chemokine CCL2
Cytokine Receptor gp130
Dander
Female
Humans
Interleukin-6
Male
Pyroglyphidae
RNA-Seq
Receptors, Interleukin-6
Respiratory Hypersensitivity
Young Adult
CCL2
IL-6
IL-6 receptor
allergy
asthma
bronchoalveolar lavage
fibroblasts
trans-signalling
Discipline(s) HAL :
Sciences du Vivant [q-bio]
Résumé en anglais : [en]
In asthma, IL-6 is a potential cause of enhanced inflammation, tissue damage and airway dysfunction. IL-6 signalling is regulated by its receptor, which is composed of two proteins, IL-6R and GP130. In addition to their ...
Lire la suite >In asthma, IL-6 is a potential cause of enhanced inflammation, tissue damage and airway dysfunction. IL-6 signalling is regulated by its receptor, which is composed of two proteins, IL-6R and GP130. In addition to their membrane form, these two proteins may be found as extracellular soluble forms. The interaction of IL-6 with soluble IL-6R (sIL-6R) can trigger IL-6 trans-signalling in cells lacking IL-6R. Conversely, the soluble form of GP130 (sGP130) competes with its membrane form to inhibit IL-6 trans-signalling. We aimed to analyse IL-6 trans-signalling proteins in the airways of subjects after an allergen challenge. We used a model of segmental bronchoprovocation with an allergen (SBP-Ag) in human subjects with allergy. Before and 48 h after SBP-Ag, bronchoalveolar lavages (BALs) allowed for the analysis of proteins in BAL fluids (BALFs) by ELISA, and membrane proteins on the surface of BAL cells by flow cytometry. In addition, we performed RNA sequencing (RNA-seq) and used proteomic data to further inform on the expression of the IL-6R subunits by eosinophils, bronchial epithelial cells and lung fibroblasts. Finally, we measured the effect of IL-6 trans-signalling on bronchial fibroblasts, in vitro. IL-6, sIL-6R, sGP130 and the molar ratio of sIL-6R/sGP130 increased in the airways after SBP-Ag, suggesting the potential for enhanced IL-6 trans-signalling activity. BAL lymphocytes, monocytes and eosinophils displayed IL-6R on their surface and were all possible providers of sIL-6R, whereas GP130 was highly expressed in bronchial epithelial cells and lung fibroblasts. Finally, bronchial fibroblasts activated by IL-6 trans-signalling produced enhanced amounts of the chemokine, MCP-1 (CCL2). After a bronchial allergen challenge, we found augmentation of the elements of IL-6 trans-signalling. Allergen-induced IL-6 trans-signalling activity can activate fibroblasts to produce chemokines that can further enhance inflammation and lung dysfunction.Lire moins >
Lire la suite >In asthma, IL-6 is a potential cause of enhanced inflammation, tissue damage and airway dysfunction. IL-6 signalling is regulated by its receptor, which is composed of two proteins, IL-6R and GP130. In addition to their membrane form, these two proteins may be found as extracellular soluble forms. The interaction of IL-6 with soluble IL-6R (sIL-6R) can trigger IL-6 trans-signalling in cells lacking IL-6R. Conversely, the soluble form of GP130 (sGP130) competes with its membrane form to inhibit IL-6 trans-signalling. We aimed to analyse IL-6 trans-signalling proteins in the airways of subjects after an allergen challenge. We used a model of segmental bronchoprovocation with an allergen (SBP-Ag) in human subjects with allergy. Before and 48 h after SBP-Ag, bronchoalveolar lavages (BALs) allowed for the analysis of proteins in BAL fluids (BALFs) by ELISA, and membrane proteins on the surface of BAL cells by flow cytometry. In addition, we performed RNA sequencing (RNA-seq) and used proteomic data to further inform on the expression of the IL-6R subunits by eosinophils, bronchial epithelial cells and lung fibroblasts. Finally, we measured the effect of IL-6 trans-signalling on bronchial fibroblasts, in vitro. IL-6, sIL-6R, sGP130 and the molar ratio of sIL-6R/sGP130 increased in the airways after SBP-Ag, suggesting the potential for enhanced IL-6 trans-signalling activity. BAL lymphocytes, monocytes and eosinophils displayed IL-6R on their surface and were all possible providers of sIL-6R, whereas GP130 was highly expressed in bronchial epithelial cells and lung fibroblasts. Finally, bronchial fibroblasts activated by IL-6 trans-signalling produced enhanced amounts of the chemokine, MCP-1 (CCL2). After a bronchial allergen challenge, we found augmentation of the elements of IL-6 trans-signalling. Allergen-induced IL-6 trans-signalling activity can activate fibroblasts to produce chemokines that can further enhance inflammation and lung dysfunction.Lire moins >
Langue :
Anglais
Comité de lecture :
Oui
Audience :
Internationale
Établissement(s) :
Université de Lille
Inserm
CHU Lille
Inserm
CHU Lille
Collections :
Date de dépôt :
2023-10-21T11:40:09Z
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