Double-stranded RNA exacerbates pulmonary allergic reaction through TLR3: implication of airway epithelium and dendritic cells
| Autor: | François Trottein, David Torres, Muriel Pichavant, Philippe Gosset, Mustapha Si-Tahar, Audrey Dieudonné, Eva Vilain, Philippe Lassalle, Bernhard Ryffel |
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| Přispěvatelé: | Biomolécules et inflammation pulmonaire, Institut Pasteur de Lille, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille, Droit et Santé, Immunologie et Embryologie Moléculaires (IEM), Université d'Orléans (UO)-Centre National de la Recherche Scientifique (CNRS), Défense innée et inflammation, Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Schistosomiase, paludisme et inflammation, Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM) |
| Jazyk: | angličtina |
| Rok vydání: | 2010 |
| Předmět: |
MESH: Signal Transduction
Chemokine viruses MESH: Mice Knockout Mice 0302 clinical medicine RNA Viral -- administration & dosage -- toxicity MESH: Respiratory Mucosa Toll-Like Receptor 3 -- deficiency -- genetics -- physiology Immunology and Allergy MESH: Animals Ovalbumin -- administration & dosage -- immunology CCL11 Mice Knockout 0303 health sciences MESH: Dendritic Cells Sciences bio-médicales et agricoles respiratory system MESH: Toll-Like Receptor 3 Respiratory Hypersensitivity -- genetics -- immunology -- pathology 3. Good health Bronchial Hyperreactivity -- genetics -- immunology -- pathology MESH: Respiratory Hypersensitivity MESH: RNA Viral RNA Double-Stranded -- administration & dosage -- toxicity RNA Viral [SDV.IMM]Life Sciences [q-bio]/Immunology Female Bronchial Hyperreactivity medicine.symptom Allergens -- administration & dosage -- immunology Signal Transduction MESH: Allergens Ovalbumin Immunology Inflammation Respiratory Mucosa Biology 03 medical and health sciences Dendritic Cells -- immunology -- pathology -- transplantation Immune system MESH: RNA Double-Stranded MESH: Mice Inbred C57BL Signal Transduction -- genetics -- immunology Respiratory Hypersensitivity medicine Animals Respiratory Mucosa -- immunology -- pathology MESH: Mice RNA Double-Stranded 030304 developmental biology MESH: Ovalbumin MESH: Bronchial Hyperreactivity Dendritic Cells MESH: Adaptor Proteins Vesicular Transport Allergens Adaptor Proteins Vesicular Transport -- deficiency -- genetics -- physiology Toll-Like Receptor 3 Mice Inbred C57BL CCL20 Adaptor Proteins Vesicular Transport Disease Models Animal TRIF TLR3 biology.protein Respiratory epithelium MESH: Disease Models Animal MESH: Female 030215 immunology |
| Zdroj: | Journal of Immunology Journal of Immunology, Publisher : Baltimore : Williams & Wilkins, c1950-. Latest Publisher : Bethesda, MD : American Association of Immunologists, 2010, 185 (1), pp.451-9. ⟨10.4049/jimmunol.0902833⟩ Journal of Immunology, 2010, 185 (1), pp.451-9. ⟨10.4049/jimmunol.0902833⟩ The Journal of immunology, 185 (1 |
| ISSN: | 0022-1767 1550-6606 |
| DOI: | 10.4049/jimmunol.0902833⟩ |
| Popis: | Respiratory viral infections have been implicated in exacerbations of allergic asthma, characterized by a Th2-biased immune response. Respiratory viruses target airway epithelial cells and dendritic cells (DCs). Their activation is, at least in part, mediated by the TLR3-dependent recognition of virus-derived dsRNA. To elucidate the role of epithelial cells and DCs and the implication of TLR3/Toll/IL-1R domain-containing adaptor-inducing IFN-beta (TRIF) pathway, we developed a mouse model of lung allergic exacerbation. The effect of intranasal administration of dsRNA in OVA-sensitized wild-type mice and TRIF(-/-) mice was evaluated on airway hyperresponsiveness and pulmonary inflammation. Our data demonstrated that treatment with dsRNA significantly increased the airway hyperresponsiveness, the lung inflammation, and the OVA-specific Th2 response. This was associated with an infiltrate of eosinophils, myeloid DCs, and T lymphocytes. TRIF activation was required for the development of dsRNA-induced exacerbation of the allergic reaction. Intratracheal transfer of IL-4/dsRNA/OVA-pretreated DCs also triggered exacerbation of the allergic reaction, whereas cells primed with dsRNA/OVA had a more limited effect. dsRNA-induced production of CCL20 by airway epithelium was associated with DC recruitment. In vivo and in vitro treatment with dsRNA amplified airway epithelial production of the pro-Th2 chemokines CCL11 and CCL17, their secretion being enhanced by Th2 cytokines. In conclusion, dsRNA derived from respiratory viruses trigger exacerbation of the pulmonary allergic reaction through TLR3/TRIF-dependent pathway. Moreover, Th2 cytokines participate in this process by modulating the response of airway epithelium and DCs to dsRNA. Journal Article Research Support, Non-U.S. Gov't SCOPUS: ar.j info:eu-repo/semantics/published |
| Databáze: | OpenAIRE |
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