The Journal of Experimental Medicine
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The Journal of Experimental Medicine, Vol 134, 136-148, Copyright © 1971 by The Rockefeller University Press

MEDIATION OF IMMUNOLOGICAL INJURY

IMMUNOLOGICAL RELEASE OF HISTAMINE AND SLOW-REACTING SUBSTANCE OF ANAPHYLAXIS FROM HUMAN LUNG : I. MODULATION BY AGENTS INFLUENCING CELLULAR LEVELS OF CYCLIC 3',5'-ADENOSINE MONOPHOSPHATE



Robert P. Orange 1, W. Gerald Austen 1, and K. Frank Austen 1

1 From the Harvard Medical School, Robert B. Brigham Hospital, Boston, Massachusetts 02120 and the Massachusetts General Hospital, Boston, Massachusetts 02114

The sensitization of human lung with atopic serum is both time and temperature dependent. Highly purified IgE myeloma protein is capable of blocking sensitization of human lung with atopic serum whereas myeloma proteins of the IgG subgroups are inactive. Drugs capable of increasing cellular levels of CAMP such as ß-adrenergic agents and methylxanthines inhibit the antigen-induced release of both histamine and SRS-A from human lung and these agents demonstrate synergism when used together. The ß-adrenergic blocking agent, propranolol, prevents epinephrine-induced inhibition of the immunologic release of the mediators. Diethylcarbamazine also inhibits the antigen-induced release of histamine and SRS-A from human lung and a synergism between this drug and epinephrine is observed. Predominantly alpha-adrenergic stimulation achieved by combining propranolol with epinephrine or norepinephrine not only prevented the inhibitory activity of the sympathomimetic amines but also resulted in an enhanced release of histamine and SRS-A. These observations suggest that whereas increases in cellular levels of CAMP are inhibitory, decreases in cellular levels of CAMP enhance the antigen-induced release of the mediators.


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