Premium
Influence of bee venom immunotherapy on degranulation and leukotriene generation in human blood basophils
Author(s) -
JUTEL MAREK,
MÜLLER U. R.,
ERICKER M.,
RIHS S.,
PICHLER W. J.,
DAHINDEN C.
Publication year - 1996
Publication title -
clinical and experimental allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.462
H-Index - 154
eISSN - 1365-2222
pISSN - 0954-7894
DOI - 10.1111/j.1365-2222.1996.tb00496.x
Subject(s) - histamine , basophil , immunoglobulin e , immunology , leukotriene , allergen , allergic response , medicine , degranulation , allergy , pharmacology , receptor , antibody , asthma
Summary Background Rapid clinical tolerance can be induced over several hours by very fast bee venom immunotherupy (VIT) protocols. Objective To investigate the mechanisms underlying VIT we examined the changes of blood basophil responsivetiess during VIT. Methods Seven bee venom allergic patients with a history of severe systemic reactions after a bee sting were investigated. A cumulative dose of 111.1 μg bee venom (BV) was administered sc over 3.5 h under intensive care conditions according to an ultra‐rush protocol. The release of histamine and the formation of leukotrienes in response to BV, major BV allergen Phospholipase A 2 (PLA), IgE receptor cross‐linking with the use of monoclonal antibodies against IgE and IgE receptor, as well as IgE independent activation in response to C5a were determined in vitro before and after ultra‐rush VIT. Results We demonstrated a decrease of total histamine in peripheral blood leucocytes just after VIT. Histamine release in response to all the stimuli used is not affected by ultra‐rush VIT, if expressed as per cent release of total histamine. However, the absolute amount of product released in response to stimulation was decreased, particularly with allergen (BV, PLA). We also found a significant reduction of LTC4 formation after VIT in samples stimulated with specific allergen (BV, PLA). Conclusion Blood basophils are a target for VIT, which induces impaired release of both preformed and newly generated mediators. However, we believe the basic mechanisms of rapid clinical tolerance induced by ultra‐rush VIT remain to be investigated.