Asthma as an inflammatory disease: implications for management.
BACKGROUND
Eosinophilic inflammation plays a central role in the pathogenesis of asthma. Striking inflammatory changes are present in the airways of patients with all levels of disease severity. The degree of airway inflammation correlates with airway hyperresponsiveness, the primary physiologic abnormality of asthma. Inflammation is typically initiated by immunologic events (including allergy) and is driven by mediators released by various cells of the immune system, particularly eosinophils, monocytes and macrophages, lymphocytes, and mast cells.


METHODS
Literature on asthma and the inflammatory response was drawn from recent articles presented and reviewed in journal clubs and from selected articles from the National Library of Medicine.


CONCLUSIONS
The inflammatory process can be divided into six steps: triggering, signaling, migration, inflammatory cell activation, tissue damage, and resolution. Recognition of the importance of inflammation in the pathogenesis of asthma and the progression of the disease has shifted research efforts and the development of new therapeutic agents toward reduction of airway inflammation. Anti-inflammatory therapy, which can be directed against specific steps in the inflammatory process, actually reduces bronchial hyperresponsiveness. Although anti-inflammatory management has assumed a primary role in asthma therapy, short acting beta 2-adrenergic receptor agonists are needed for treatment of acute symptoms, and some patients require regular beta 2-agonist therapy despite apparently adequate anti-inflammatory therapy.
Dolen
W K
WK
Department of Pediatrics, Medical College of Georgia, Augusta 30912, USA.
D000280:Administration, Inhalation; D000305:Adrenal Cortex Hormones / Q000008:administration & dosage; D001249:Asthma / Q000188:drug therapy / Q000276:immunology*; D001980:Bronchi / Q000276:immunology; D016535:Bronchial Hyperreactivity / Q000188:drug therapy / Q000276:immunology; D004802:Eosinophilia / Q000188:drug therapy / Q000276:immunology*; D004848:Epithelium / Q000276:immunology; D006801:Humans; D007111:Immunity, Cellular / Q000187:drug effects / Q000276:immunology; D018836:Inflammation Mediators / Q000502:physiology*; D012130:Respiratory Hypersensitivity / Q000188:drug therapy / Q000276:immunology*
D000305:Adrenal Cortex Hormones; D018836:Inflammation Mediators