2.50
Hdl Handle:
http://hdl.handle.net/2336/47303
Title:
Asthma: an inflammatory mediator soup
Authors:
Bjornsdottir, U S; Cypcar, D M
Citation:
Allergy 1999, 54 Suppl 49:55-61
Issue Date:
1-Mar-1999
Abstract:
Reversible or partially reversible airway obstruction, inflammation, and bronchial hyperresponsiveness to various stimuli are the defining characteristics of asthma. Airway obstruction in asthma is a complex event that is due to bronchospasm, inflammation, and mucus formation. Inflammation has assumed a more central role in the pathogenesis of the disease, as it contributes not only to airflow obstruction, but also to bronchial hyperresponsiveness. The inciting trigger, or inhaled allergen, in asthma induces the activation of mast cells and macrophages with the subsequent release of several proinflammatory mediators, including leukotrienes, chemotactic factors, and cytokines. Antigen processed by macrophages is presented to undifferentiated T helper cells, inducing differentiation to the Th2 phenotype, with the subsequent release of IL-4 and IL-5, causing IgE synthesis and eosinophil infiltration, respectively. Macrophage-derived cytokines, such as IL-1, TNF-alpha, and IFN-gamma, activate endothelial cells, upregulating the expression of adhesion molecules such as ICAM-1 and VCAM-1, which permit egression of leukocytes from the vasculature to the airway mucosa. Several inflammatory cells, such as eosinophils, mast cells, and macrophages, not only cause airway damage, but also synthesize cytokines that perpetuate the inflammatory process. This complex interplay of inflammatory cells and mediators causes the classic histopathophysiologic features in the airways of both symptomatic and asymptomatic individuals with asthma, emphasizing the importance of early recognition and antiinflammatory treatment.
Description:
To access publisher full text version of this article. Please click on the hyperlink in Additional Links field
Additional Links:
http://dx.doi.org/10.1111/j.1398-9995.1999.tb04389.x

Full metadata record

DC FieldValue Language
dc.contributor.authorBjornsdottir, U S-
dc.contributor.authorCypcar, D M-
dc.date.accessioned2009-01-12T15:03:24Z-
dc.date.available2009-01-12T15:03:24Z-
dc.date.issued1999-03-01-
dc.date.submitted2009-01-12-
dc.identifier.citationAllergy 1999, 54 Suppl 49:55-61en
dc.identifier.issn0105-4538-
dc.identifier.pmid10422749-
dc.identifier.doi10.1111/j.1398-9995.1999.tb04389.x-
dc.identifier.urihttp://hdl.handle.net/2336/47303-
dc.descriptionTo access publisher full text version of this article. Please click on the hyperlink in Additional Links fielden
dc.description.abstractReversible or partially reversible airway obstruction, inflammation, and bronchial hyperresponsiveness to various stimuli are the defining characteristics of asthma. Airway obstruction in asthma is a complex event that is due to bronchospasm, inflammation, and mucus formation. Inflammation has assumed a more central role in the pathogenesis of the disease, as it contributes not only to airflow obstruction, but also to bronchial hyperresponsiveness. The inciting trigger, or inhaled allergen, in asthma induces the activation of mast cells and macrophages with the subsequent release of several proinflammatory mediators, including leukotrienes, chemotactic factors, and cytokines. Antigen processed by macrophages is presented to undifferentiated T helper cells, inducing differentiation to the Th2 phenotype, with the subsequent release of IL-4 and IL-5, causing IgE synthesis and eosinophil infiltration, respectively. Macrophage-derived cytokines, such as IL-1, TNF-alpha, and IFN-gamma, activate endothelial cells, upregulating the expression of adhesion molecules such as ICAM-1 and VCAM-1, which permit egression of leukocytes from the vasculature to the airway mucosa. Several inflammatory cells, such as eosinophils, mast cells, and macrophages, not only cause airway damage, but also synthesize cytokines that perpetuate the inflammatory process. This complex interplay of inflammatory cells and mediators causes the classic histopathophysiologic features in the airways of both symptomatic and asymptomatic individuals with asthma, emphasizing the importance of early recognition and antiinflammatory treatment.en
dc.language.isoenen
dc.publisherBlackwell Munksgaarden
dc.relation.urlhttp://dx.doi.org/10.1111/j.1398-9995.1999.tb04389.xen
dc.subject.meshAsthmaen
dc.subject.meshCell Adhesion Moleculesen
dc.subject.meshCell Movementen
dc.subject.meshCytokinesen
dc.subject.meshEosinophilsen
dc.subject.meshEpithelial Cellsen
dc.subject.meshHumansen
dc.subject.meshInflammation Mediatorsen
dc.subject.meshT-Lymphocytes, Helper-Induceren
dc.titleAsthma: an inflammatory mediator soupen
dc.typeArticleen
dc.contributor.departmentPulmonary Department, University Hospital of Iceland, Vifilstadir.en
dc.identifier.journalAllergyen
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