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Published on: January 21, 2018
Increased complement-mediated leukocytic histamine release in atopics
Complement-mediated leukocytic histamine release was compared in normal and atopic subjects using isolated leukocytes or heparinized blood. Leukocytes were treated with zymosan-activated autologous serum, whereas blood was directly incubated with zymosan particles. Histamine released from basophils into the leukocyte supernatant or plasma was measured spectrofluorometrically and expressed in percent of total histamine. In atopics, the mean histamine release (47% for leukocytes and 12% for blood) was significantly higher than in normals (30% and 5%, respectively). Individual variations were large in both groups, and a good concordance was noted between the two techniques. By cross-experiments using activated isologous serum from AB donors instead of autologous serum, it was demonstrated that individual variability was not due to differences in intensity of complement activation. Passive sensitization of normal leukocytes with IgE antibodies increased their ability to release histamine in the presence of activated serum. Thus, high complement-mediated leukocytic histamine release is more commonly found in atopics, and appears to be secondary to an intrinsic abnormality of basophils. It is suggested that complement activation and subsequent inflammation could play, especially in house dust-caused asthma, a more important role than previously appreciated. Moreover, an exaggerated mediator releasability as may occur even in nonatopic subjects, could possibly explain some predisposition to interstitial pulmonary diseases caused by inhalants capable of activating complement.
Complement-mediated leukocytic histamine release was compared in normal and atopic subjects using isolated leukocytes or heparinized blood. Leukocytes were treated with zymosan-activated autologous serum, whereas blood was directly incubated with zymosan particles. Histamine released from basophils into the leukocyte supernatant or plasma was measured spectrofluorometrically and expressed in percent of total histamine. In atopics, the mean histamine release (47% for leukocytes and 12% for blood) was significantly higher than in normals (30% and 5%, respectively). Individual variations were large in both groups, and a good concordance was noted between the two techniques. By cross-experiments using activated isologous serum from AB donors instead of autologous serum, it was demonstrated that individual variability was not due to differences in intensity of complement activation. Passive sensitization of normal leukocytes with IgE antibodies increased their ability to release histamine in the presence of activated serum. Thus, high complement-mediated leukocytic histamine release is more commonly found in atopics, and appears to be secondary to an intrinsic abnormality of basophils. It is suggested that complement activation and subsequent inflammation could play, especially in house dust-caused asthma, a more important role than previously appreciated. Moreover, an exaggerated mediator releasability as may occur even in nonatopic subjects, could possibly explain some predisposition to interstitial pulmonary diseases caused by inhalants capable of activating complement.
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