Neutrophils and mast cells. I. Human neutrophil-derived histamine- releasing activity

• Published in: The Journal of immunology (1950) Vol. 139; no. 5; pp. 1624 - 1630
• Main Authors: White, MV, Kaliner, MA
• Format: Journal Article
• Language: English
• Published: Bethesda, MD Am Assoc Immnol 01.09.1987; American Association of Immunologists
• Subjects: Animals; Basophils - drug effects; Basophils - secretion; Biological and medical sciences; Female; Fundamental and applied biological sciences. Psychology; Fundamental immunology; Histamine Release; Humans; Immediate hypersensitivity. Allergy. Anaphylaxis, etc; Immunobiology; Leukemia, Experimental; Male; Mast Cells - secretion; Neutrophils - secretion; Rats; Reaction mechanisms, antibodies, chemical mediators; Tetradecanoylphorbol Acetate - pharmacology; Human; Allergy; Histamine; Neutrophile; Basophile; Inflammation; Mast cell; Release
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.139.5.1624

Histamine release occurs during the late phase allergic reaction concomitantly with neutrophil (PMN) infiltration. To determine whether PMN might release a factor capable of causing histamine release, supernatants generated by incubating human PMN in the presence or absence of specific activators were added to rat basophilic leukemia cells (RBL) and histamine release was measured. PMN supernatants from 17 of 21 donors induced noncytotoxic histamine release. Neutrophil-derived histamine-releasing activity, termed HRA-N, was dose-dependent and supernatants from greater than or equal to 10(7) PMN/ml caused 6 to 27% net histamine release from RBL. PMN supernatants induced histamine release as effectively as did intact PMN cocultured with RBL. The capacity of various donors to generate HRA-N was not related to atopic status or gender but was inversely related to the proportion of eosinophils (EOS) contaminating the PMN isolate (the larger the proportion of EOS, the lower the histamine release). Addition of EOS to PMN during the generation of HRA-N completely inhibited histamine-releasing activity. HRA-N was not released from mononuclear cells or platelets contaminating the PMN preparation. HRA-N release was not increased by the presence of either serum-treated zymosan or phorbol myristate acetate, agents that caused dose-related release of PMN granule enzymes. Indeed, HRA-N was released from unstimulated PMN in the complete absence of granule enzyme release. HRA-N release was detectable by 15 min and the majority of release occurred between 45 and 60 min of incubation. Thus, the data indicate that HRA-N is released spontaneously from human PMN and that HRA-N release is independent of primary or secondary PMN granule release. It is attractive to suggest that release of HRA-N by PMN might act to recruit mast cells or basophils into participating in acute inflammatory reactions.