The aim of our work was to investigate the effect of histamine releasing factor (HRF), produced in vitro by lymphocytes obtained from atopic and non-atopic asthmatics, on mast cells of various species (mouse - peritoneal mast cells, hamster and rat - peritoneal and pleural mast cells, guinea-pig - mesenteric and pulmonary mast cells). We found that human HRF is able to release histamine from the examined mast cell populations in a dose-dependent fashion. Mast cells from various species differed in their susceptibility to the action of HRF; rat pleural and guinea-pig mesenteric and pulmonary mast cells were the most susceptible, while mouse and hamster peritoneal mast cells - the least susceptible. The presence of 50% D2O in the medium significantly increased HRF-induced histamine release from rat mast cells, while the addition of phosphatidylserine did not change it. HRF-induced histamine release from guinea-pig mesenteric mast cells was not related to sensitization of these cells. We also compared histamine release from guinea-pig pulmonary and mesenteric mast cells induced by human HRF produced in vitro by lymphocytes obtained from atopic and non-atopic asthmatics. We have found that supernatant from atopic asthmatics lymphocyte cultures released significantly more histamine than supernatant from non-atopic asthmatics lymphocyte cultures. Our studies give evidence that human HRF acts across the species barrier and induces histamine release from mast cells of various species. The mechanism of HRF action on mast cells seems to be different from that of allergen.
The histamine-releasing capability of Staphylococcus aureus antigens was examined in human adenoidal and mesenteric mast cells obtained by enzymic dispersion of tissues from non-allergic patients. Both populations of mast cells released histamine after challenge with bacterial protein in concentrations between 5-500 micrograms/ml. The release was dependent on the dose, temperature and metabolic energy. The maximum release was observed at 15 min after challenge. The present results suggest that Staphylococcus aureus antigens release histamine from human adenoidal and mesenteric mast cells via a non-cytotoxic, active secretory process.
Since recent studies have emphasized that mast cells from different tissues within a given species may exhibit marked differences in their functional properties, we have now examined the effect of some immunological and non-immunological histamine releasers on human mesenteric mast cells. The mesentery derived from the patients subjected to gall-bladder surgery was dispersed by collagenase (concentration of enzyme--1 mg/ml, time of incubation--90 min, 37 degrees C). The mesenteric cell suspension contained about 2% mast cells as identified by staining with toluidine blue. We observed that the mesenteric mast cells released histamine when challenged with anti-human IgE, but marked individual variations were observed. These cells had a low sensitivity to challenge with Concanavalin A and compound 48/80 (histamine release about 6%), but responded to ionophore A23187 and polymyxin B (histamine release up to 24% and 22% respectively).
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