Pathophysiology of allergic inflammation
Identifieur interne : 000075 ( Main/Exploration ); précédent : 000074; suivant : 000076Pathophysiology of allergic inflammation
Auteurs : Peter J. Barnes [Royaume-Uni]Source :
- Immunological Reviews [ 0105-2896 ] ; 2011-07.
English descriptors
- Teeft :
- Acad, Acetylation, Activates, Airway, Airway diseases, Airway epithelial cells, Airway epithelium, Airway hyperresponsiveness, Allergen, Allergen challenge, Allergic, Allergic airway, Allergic asthma, Allergic disease, Allergic diseases, Allergic response, Allergic rhinitis, Allergy, Allergy clin immunol, Allergy clin immunol maneechotesuwan, Animal models, Apc, Arachidonic acid, Asthma, Asthmatic, Asthmatic airways, Asthmatic patients, Atopic, Atopic dermatitis, Aureus, Autoantibody, Basophil, Bronchial biopsies, Cell differentiation, Chemokines, Chronic rhinosinusitis, Clin, Complex interplay, Corticosteroid, Corticosteroid resistance, Cortisol, Crit, Critical role, Curr, Curr opin allergy clin immunol, Cytokine, Cytokine genes, Dendritic, Dendritic cells, Dermatitis, Disease severity, Endogenous, Enterotoxin, Eosinophil, Eosinophilic, Epithelial, Epithelial cells, Gata3, Gata3 expression, Gene expression, Gene transcription, Growth factor, High doses, Histamine, Histone, Hyperresponsiveness, Immune, Immunoglobulin, Immunol, Important role, Important source, Inhaled, Inhaled allergen, Intrinsic asthma, John wiley sons, Keratinocytes, Kinase, Lipid, Lipid mediators, Lower airways, Lymphocyte, Lymphopoietin, Macrophage, Mast, Mast cells, Mediator, Methylation, Mucosal, Mucosal mast cells, Mucosal surfaces, Mucus, Mucus secretion, Murine, Murine model, Muscle cells, Nasal, Nasal blockage, Nasal polyps, Nerve growth factor, Neuropeptides, Neurotrophins, Neutrophil, Nitric, Nitric oxide, Normal subjects, Oral corticosteroids, Other cells, Oxidative, Oxidative stress, Pathophysiology, Pathway, Pharmacol, Plasma exudation, Potent vasodilator, Proc, Proc natl acad, Prostaglandin, Pulmonary disease, Reactive oxygen species, Receptor, Receptor antagonist, Respir, Respir cell, Respir crit care, Reviews barnes, Rhinitis, Secretion, Sensory nerves, Several cytokines, Several mediators, Severe asthma, Signal transducer, Social stress, Sputum, Staphylococcal, Staphylococcal superantigens, Stat6, Stromal, Structural cells, Superantigens, Thymic, Thymic stromal lymphopoietin, Transcription, Transcription factor, Transcription factors, Treg function, Tregs, Trends pharmacol, Tslp, Vasodilatation.
Abstract
Summary: Allergic inflammation is due to a complex interplay between several inflammatory cells, including mast cells, basophils, lymphocytes, dendritic cells, eosinophils, and sometimes neutrophils. These cells produce multiple inflammatory mediators, including lipids, purines, cytokines, chemokines, and reactive oxygen species. Allergic inflammation affects target cells, such as epithelial cells, fibroblasts, vascular cells, and airway smooth muscle cells, which become an important source of inflammatory mediators. Sensory nerves are sensitized and activated during allergic inflammation and produce symptoms. Allergic inflammatory responses are orchestrated by several transcription factors, particularly NF‐κB and GATA3. Inflammatory genes are also regulated by epigenetic mechanisms, including DNA methylation and histone modifications. There are several endogenous anti‐inflammatory mechanisms, including anti‐inflammatory lipids and cytokines, which may be defective in allergic disease, thus amplifying and perpetuating the inflammation. Better understanding of the pathophysiology of allergic inflammation has identified new therapeutic targets but developing effective novel therapies has been challenging. Corticosteroids are highly effective with a broad spectrum of anti‐inflammatory effects, including epigenetic modulation of the inflammatory response and suppression of GATA3.
Url:
DOI: 10.1111/j.1600-065X.2011.01020.x
Affiliations:
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doses</term><term>Histamine</term><term>Histone</term><term>Hyperresponsiveness</term><term>Immune</term><term>Immunoglobulin</term><term>Immunol</term><term>Important role</term><term>Important source</term><term>Inhaled</term><term>Inhaled allergen</term><term>Intrinsic asthma</term><term>John wiley sons</term><term>Keratinocytes</term><term>Kinase</term><term>Lipid</term><term>Lipid mediators</term><term>Lower airways</term><term>Lymphocyte</term><term>Lymphopoietin</term><term>Macrophage</term><term>Mast</term><term>Mast cells</term><term>Mediator</term><term>Methylation</term><term>Mucosal</term><term>Mucosal mast cells</term><term>Mucosal surfaces</term><term>Mucus</term><term>Mucus secretion</term><term>Murine</term><term>Murine model</term><term>Muscle cells</term><term>Nasal</term><term>Nasal blockage</term><term>Nasal polyps</term><term>Nerve growth factor</term><term>Neuropeptides</term><term>Neurotrophins</term><term>Neutrophil</term><term>Nitric</term><term>Nitric 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lymphopoietin</term><term>Transcription</term><term>Transcription factor</term><term>Transcription factors</term><term>Treg function</term><term>Tregs</term><term>Trends pharmacol</term><term>Tslp</term><term>Vasodilatation</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract">Summary: Allergic inflammation is due to a complex interplay between several inflammatory cells, including mast cells, basophils, lymphocytes, dendritic cells, eosinophils, and sometimes neutrophils. These cells produce multiple inflammatory mediators, including lipids, purines, cytokines, chemokines, and reactive oxygen species. Allergic inflammation affects target cells, such as epithelial cells, fibroblasts, vascular cells, and airway smooth muscle cells, which become an important source of inflammatory mediators. Sensory nerves are sensitized and activated during allergic inflammation and produce symptoms. Allergic inflammatory responses are orchestrated by several transcription factors, particularly NF‐κB and GATA3. Inflammatory genes are also regulated by epigenetic mechanisms, including DNA methylation and histone modifications. There are several endogenous anti‐inflammatory mechanisms, including anti‐inflammatory lipids and cytokines, which may be defective in allergic disease, thus amplifying and perpetuating the inflammation. Better understanding of the pathophysiology of allergic inflammation has identified new therapeutic targets but developing effective novel therapies has been challenging. Corticosteroids are highly effective with a broad spectrum of anti‐inflammatory effects, including epigenetic modulation of the inflammatory response and suppression of GATA3.</div></front></TEI><affiliations><list><country><li>Royaume-Uni</li></country><region><li>Angleterre</li><li>Grand Londres</li></region><settlement><li>Londres</li></settlement></list><tree><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Barnes, Peter J" sort="Barnes, Peter J" uniqKey="Barnes P" first="Peter J." last="Barnes">Peter J. Barnes</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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