IGE-MEDIATED LATE PHASE REACTIONS - THE PATHO-PHYSIOLOGIC BACKGROUND OF CHRONIC BRONCHIAL ASTHMA?

Abstract

Late phase reactions (LPR) have been considered generally as type III allergy according to the classification of Coombs and Gell. IgE-antibodies, however, are able to initiate not only immediate, but also late cutaneous reactions (LCR). Using the skin blister technique we could show LCR to be mediated by inflammatory mediators generated during the preceeding immediate reaction. Various mediators as histamine, active kallikrein, platelet activating properties, leukotrienes and thromboxanes were demonstrable in skin blister fluids their concentration being in part related to the time course of the skin reactions. LCRs were diminished by eikosatetraynoic acid (not by indomethacin), by dazoxiben as well as by ethanolic onion extract. Betamimetics as salbutamol and anticholinergics as ipratropiumbromide could reverse late bronchial reactions (LBR), ethanolic onion extract could prevent LBR. Other authors found prostaglandin D2 and chemotactic substances during LPR as well as protective effects of corticosteroids, disodium cromoglicicum, tranexamic acid and combined histamine H1/H2 receptor antagonists. Two types of LPR have to be distinguished: type I and type III. The further is initiated by a IgE-dependent mast cell degranulation and maintained by a complex inter action of mediators and cells. It represents the patho-physiolggic correlate of long lasting bronchial asthma.