Neutrophils and mast cells. Comparison of neutrophil-derived histamine-releasing activity with other histamine-releasing factors.
Human neutrophil-derived histamine-releasing activity (HRA-N) was partially purified and found to contain a heat-stable 1400 to 2300-Da fraction which caused human basophils and rat basophil leukemia cells (RBL) to degranulate. The capacity of HRA-N to activate basophils was not related to the gender or atopic status of the basophil donor, but was related to anti-IgE responsiveness. Several lines of evidence suggest that HRA-N and anti-IgE induce histamine release through distinctly different mechanisms: 1) the time course of HRA-N- and anti-IgE-induced RBL histamine release are different; 2) HRA-N causes histamine release from RBL with and without surface-bound IgE; 3) lactic acid stripping of IgE from human basophils reduces anti-IgE-induced histamine release, but has no consistent effect on HRA-N-induced histamine release; and 4) passive sensitization of lactic acid-stripped basophils with IgE restores anti-IgE-induced histamine release but not HRA-N-induced histamine release. Several histamine-releasing factors (HRF) were compared with HRA-N. Human nasal HRF (HRF-NW, crude and partially purified fractions of 15 to 30, 3.5 to 9, and less than 3.5 kDa), like HRA-N, caused equal histamine release from both native and IgE-sensitized RBL. However, only the 15- to 30-kDa fraction caused histamine release from human basophils in the doses tested. Mononuclear cell HRF (HRF-M, crude and a partially purified 25 kDa Mr fraction) and platelet HRF (HRF-P, crude preparation) failed to cause histamine release from either native or IgE-sensitized RBL but caused 30 +/- 5.5% and 20 +/- 10% net histamine release from human basophils, respectively. HRA-N and HRF-NW were both stable to boiling. These data, taken together, suggest that the capacity of HRA-N to induce RBL and human basophil histamine release and of HRF-NW to stimulate RBL histamine release is independent of IgE. The data further suggest that HRA-N and HRF-NW can be distinguished by size, and that they both differ from mononuclear cell HRF and platelet HRF. Thus, it appears that inflammatory cells generate a family of distinct HRF.
White
M V
MV
National Institute of Allergy and Infectious Disease, Laboratory of Clinical Investigation, Bethesda, MD 20892.
Kaplan
A P
AP
Haak-Frendscho
M
M
Kaliner
M
M
D000818:Animals; D001491:Basophils / Q000276:immunology*; D014408:Biomarkers, Tumor; D001792:Blood Platelets / Q000032:analysis / Q000276:immunology; D002460:Cell Line; D004355:Drug Stability; D006636:Histamine Release / Q000187:drug effects*; D006358:Hot Temperature; D006801:Humans; D007073:Immunoglobulin E / Q000502:physiology; D007773:Lactates; D019344:Lactic Acid; D007938:Leukemia / Q000276:immunology; D008222:Lymphokines / Q000502:physiology; D009297:Nasal Mucosa / Q000032:analysis / Q000276:immunology; D009504:Neutrophils / Q000032:analysis / Q000276:immunology*; D051381:Rats; D000090324:Tumor Protein, Translationally-Controlled 1
D014408:Biomarkers, Tumor; D007773:Lactates; D008222:Lymphokines; D000090324:Tumor Protein, Translationally-Controlled 1; D019344:Lactic Acid; D007073:Immunoglobulin E