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Effects of PBMC‐derived histamine‐releasing factors on histamine release from human skin and lung mast cells
Author(s) -
OKAYAMA Y.,
BRZEZIŃSKABŁASZCZYK E.,
KUNA P.,
KAPLAN A. P.,
CHURCH M. K.
Publication year - 1995
Publication title -
clinical and experimental allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.462
H-Index - 154
eISSN - 1365-2222
pISSN - 0954-7894
DOI - 10.1111/j.1365-2222.1995.tb00032.x
Subject(s) - histamine , mast cell , chemistry , peripheral blood mononuclear cell , monocyte , pharmacology , immunology , endocrinology , biochemistry , biology , in vitro
Summary Background: A field of study which has attracted much recent interest is the ability of mononuclear cells and neutrophils to interact with hislamine releasing cells by production of specific histamine releasing factors (HRFs). However, almost all of these studies have been performed on basophils rather than human mast ceils. Objective: We have investigated the effects of lyophilized fractions of HRF preparations on histamine release from human skin and lung mast cells. Methods: Lyophilized fractions of HRF preparations include crude supernatant from mononuclear cell/platelet (crude), void peak from union exchange chromatography column (void), second peak from anion exchange chromatography (peak 2), neutrophil‐activating peptide‐2 (NAP‐2), which was purified from void peak at molecular weight of 8‐12 kDa, and monocyte chemotactic‐activating factor (MCAF). Mast cells were enzymatically dispersal. Results: Crude (24.2 μ g/mL‐2.42mg/mL), void (5.4 μ g/mL‐0.54mg/mL). peak 2 (3.5 μ g/mL‐0.35mg/tnL), and NAP‐2 (1‐20 μ g/mL) failed to release hislamine from lung mast cells. In skin mast cells, only higher concentrations of crude and void caused minimal release of histamine. MCAF up to micromolar concentrations failed to have an effect on mast cells from either source, However, these HRFs induced histamine release from human basophils. We also explored whether HRFs and stem cell factor could act as either priming agents for each other or for anti‐IgE. The response of skin mast cells to all these preparations was not enhanced by preincubation in stem cell factor at 1 ng/mL. nor did the HRFs and MCAF enhance the response of skin mast cells to anti‐IgE. Conclusion: These results suggest that these HRFs have no significant effect on dispersed human cutaneous and lung mast cells.