Late asthmatic responses: inquiry into mechanisms and significance.
Late asthmatic responses are common, simulate a chronic phase of asthma, and are associated with an influx of inflammatory cells. The precise sequence of events leading to late inflammatory responses and increased hyperresponsiveness of the airways is uncertain, but likely begins with the triggering of mediator release from local (luminal or interstitial) mast cells or, conceivably, alveolar macrophages. Consequent influx and activation of granulocytes, including eosinophils and neutrophils, possibly T lymphocytes, basophils, and platelets, and subsequently later-arriving monocytes and macrophages, may be responsible for a continuing inflammatory reaction, airways hyperresponsiveness, and continuing active bronchial asthma. Identification of the relative importance of responsible cells and mediators will help clarify pathogenesis of bronchial asthma and should lead to a better understanding and design of therapeutic regimens and preventive measures in the management of this common and important disease.
D000403:Airway Resistance; D001249:Asthma / Q000503:physiopathology*; D001792:Blood Platelets / Q000276:immunology; D001980:Bronchi / Q000503:physiopathology; D006098:Granulocytes / Q000276:immunology; D006801:Humans; D006967:Hypersensitivity / Q000276:immunology; D006968:Hypersensitivity, Delayed / Q000276:immunology; D007073:Immunoglobulin E / Q000276:immunology; D007074:Immunoglobulin G / Q000276:immunology; D007249:Inflammation / Q000276:immunology; D008264:Macrophages / Q000276:immunology; D008407:Mast Cells / Q000276:immunology; D009784:Occupational Diseases / Q000276:immunology; D013997:Time Factors
D007074:Immunoglobulin G; D007073:Immunoglobulin E