Histamine release from human leukocytes: modulation by a cytochalasin B-sensitive barrier

Harvey R. Colten; Kenneth H. Gabbay

doi:10.1172/JCI106998

^{Division of Allergy, Department of Medicine, Children's Hospital Medical Center, Boston, Massachusetts 02115}

^{Division of Immunology, Department of Medicine, Children's Hospital Medical Center, Boston, Massachusetts 02115}

^{Division of Endocrinology, Department of Medicine, Children's Hospital Medical Center, Boston, Massachusetts 02115}

^{Department of Pediatrics, Harvard Medical School, Boston, Massachusetts 02115}

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^{Division of Allergy, Department of Medicine, Children's Hospital Medical Center, Boston, Massachusetts 02115}

^{Division of Immunology, Department of Medicine, Children's Hospital Medical Center, Boston, Massachusetts 02115}

^{Division of Endocrinology, Department of Medicine, Children's Hospital Medical Center, Boston, Massachusetts 02115}

^{Department of Pediatrics, Harvard Medical School, Boston, Massachusetts 02115}

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Published July 1, 1972 - More info

Published in Volume 51, Issue 7 on July 1, 1972
J Clin Invest. 1972;51(7):1927–1931. https://doi.org/10.1172/JCI106998.
© 1972 The American Society for Clinical Investigation

Published July 1, 1972 - Version history

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Abstract

Cytochalasin B, a metabolic product of several fungi, enhances up to 10-fold the sensitivity and reactivity of human leukocytes to antigen E or anti-IgE-mediated histamine release. The effect of cytochalasin B is a result of its action on the second, antigen-independent, stage of histamine release. These data suggest that normally, antigen-triggered histamine release is modulated by a cytochalasin-sensitive barrier (CSB). This CSB modulation of histamine release can be separated from the modulating effect of cyclic adenosine monophosphate (AMP).