Open AccessRegulation of human basophil activation; the role of Na + and Ca 2+ in IL‐3‐induced potentiation of IgE‐mediated histamine release from human basophils
Author(s) -
BEAUVAIS F.,
ECHASSERIEAU K.,
BURTIN C.,
BENVENISTE J.
Publication year - 1994
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1994.tb06035.x
Subject(s) - histamine , long term potentiation , immunology , basophil , immunoglobulin e , basophil activation , biology , chemistry , endocrinology , antibody , receptor , biochemistry
SUMMARY The release of mediators from human basophils is strongly enhanced by lL‐3. However, the signalling pathways of IL‐3 arc poorly defined in these cells. Since external Ca 2+ and Na + play important regulating roles in histamine release, the possibility that these cations could be involved in the potentiation by rL‐3 of the anti‐IgE‐induced histamine release from human basophils was considered, and it was observed that: (i) lL‐3 dramatically decreased the external Ca 2+ requirement for IgE‐mediated histamine release. However, histamine release from IL‐3‐treated basophils became only partially independent of external Ca 2+ , since addition of EGTA in the external medium abolished the effect of IL‐3; (ii) decreasing Na + influx by lowering external Na + concentration in isosmotic medium inhibited thepotenEiatiiigefTeLtoriL‐3on IgE‐mediated release; (iii) amiloride. An inhibitor of Na + /Ca 2+ and Na + /H + exchanges, and its derivative, benzamil, more specific for Na + /Ca 2+ exchanges, inhibited the release potentiated by IL‐3. In contrast, the amiloride derivative 5‐(N, N‐dimethy1)‐amiloride more specific for Na + /H + exchanges, slightly increased the IL‐3‐enhaneed release. Thus, the decreased requirement for external Ca 2+ and the dependence on external Na + taken with the effect of the Na + /Ca 2+ exchange inhibitors, suggest that Na + /Ca 2+ exchanges are involved in the IL‐3‐indueed enhancement of IgE‐mediated human basophil histamine release.