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Modulation of human leukocyte histamine release by sn‐1,2‐isopropylidene‐3‐decanoyl‐glycerol and decanoic acid cyclopentyl methylester in comparison with effects of synthetic diacylglycerols and a phorbol ester
Author(s) -
Bergstrand H.,
Lundquist B.,
Michelsen P.
Publication year - 1989
Publication title -
allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.363
H-Index - 173
eISSN - 1398-9995
pISSN - 0105-4538
DOI - 10.1111/j.1398-9995.1989.tb00439.x
Subject(s) - histamine , secretagogue , chemistry , phorbol , protein kinase c , liberation , biochemistry , melittin , endocrinology , pharmacology , medicine , kinase , in vitro , receptor , biology , peptide
Previous studies have shown that the glyceride derivative, sn‐1,2 ‐isopropylidene‐3‐decanoyl‐glycerol (IpOCOC 9 ), can trigger human leukocyte histamine release. Approximately 25 % of the total cellular histamine content is extruded in the presence of 206 # of IpOCOC 9 ; at 69 μM, however, the secretagogue action of the compound is marginal. The characteristics of the release induced by IpOCOC 9 are closely similar to those reportedly recorded at hyperosmolar triggering of basophils with mannitol, and in many respects they also mimic those observed at phorbol ester‐induced histamine release. The compound decanoic acid cyclopentyl methylester (DACPME), a structural analogue of IpOCOC 9 , fails to induce histamine release. IpOCOC 9 , but not DACPME, stimulates human polymorphonuclear leukocyte cytosolic Ca 2+− and phospholipid‐dependent his‐tone III‐S kinase activity (unpublished observations). The secretagogue action of IpOCOC 9 , has therefore tentatively, at least partly, been attributed to a direct protein kinase C activation. In the present studies, we examined the influence of IpOCOC 9 and DACPME on histamine release triggered by an ensuing exposure to anti‐IgE, the calcium ionophore A23187, formyl‐methionyl‐leucyl‐phenylalanine (EMLP), or 4β‐phor‐bol 12‐myristate 13‐acetate (PMA). It is shown that IpOCOC 9 ‐treatment of cells results in either enhancement or reduction of the release induced by anti‐IgE or by A23187, whereas FMLP‐induced release is consistently reduced and PMA‐induced release consistently enhanced by such a treatment. Treatment of cells with DACPME enhances but does not reduce anti‐IgE‐triggered release, whereas EMLP‐induced release is not affected. Pretreatment of the cells with other putative protein kinase C activators like PMA, sn‐1‐oleoyl‐2‐acetyl‐glycerol (OAC), 1,2‐dioctanoyl‐glycerol (DiCg) or the glycerol derivative sn‐1,2‐diacetyl‐3‐decanoyl‐glycerol (DiC2OCOC 9 ) affects secretagogue‐induced basophil histamine release according to specific patterns similar to but not identical with those recorded for IpOCOC 9 and DACPME. Thus, e.g., DiC 2 OCOC 9 consistently reduces but does not enhance anti‐IgE‐triggered release. These data show that limited structural changes of IpOCOC 9 may qualitatively affect its modulating properties in the human basophil histamine release system.