[Biochemical aspects of the pathogenesis of the asthma syndrome].
The induction of asthma is more easily understood by the increasing knowledge of intercellular interactions. It is obvious that a major role for the initiation of extrinsic and mixed form asthma is attributed to IgE-immunoglobulin, which after interaction with the appropriate antigen leads to the release of preformed and newly generated mediators (e.g. leukotriene with chemotactic and spasmogenic [SRS] properties) from mast cells and basophils. The latter mediators are also released from polymorphonuclear neutrophils and macrophages in the course of bacterial adherence, phagocytosis, by bacterial toxins, and via anaphylatoxin dependent mechanisms. It appears likely that the induction of intrinsic asthma might be triggered by these mediators also during viral adsorption and penetration. The interdependency of cellular reactions might be responsible for the complexity of the disease process in asthma.
D000707:Anaphylaxis / Q000276:immunology; D001249:Asthma / Q000209:etiology* / Q000276:immunology; D001491:Basophils / Q000276:immunology; D002450:Cell Communication; D002462:Cell Membrane / Q000276:immunology; D006801:Humans; D007111:Immunity, Cellular; D007073:Immunoglobulin E / Q000096:biosynthesis / Q000502:physiology; D008407:Mast Cells / Q000276:immunology; D009504:Neutrophils / Q000276:immunology; D011970:Receptors, Histamine H2; D013189:SRS-A / Q000096:biosynthesis; D013577:Syndrome
D011970:Receptors, Histamine H2; D013189:SRS-A; D007073:Immunoglobulin E
Biochemische Aspekte der Pathogenese des Asthmasyndroms.