Induction of mast cell secretion by parathormone
ABSTRACT The biologically active fragment of human parathormone (PTH) and intact bovine PTH were found to induce secretion of both serotonin and histamine from rat peritoneal mast cells in vitro. Release of serotonin and histamine was demonstrated with 25 units/ml PTH or higher. This level is within the higher limits of the elevated PTH levels found in advanced uremia. Mast cell secretion by PTH was dose, time and energy dependent and was not cytotoxic. Although mast cell activation was independent of extracellular calcium, it required intracellular calcium, thus resembling the action of certain other peptide secretagogues. Intradermal injection of PTH induced immediate increases in vascular permeability suggesting that PTH could induce mast cell secretion in vivo. Light and electron microscopic observations confirmed mast cell degranulation by exocytosis. These results demonstrate that elevated levels of PTH can induce mast cell secretion in vitro and in vivo and suggest a possible role for mast cells in the pathophysiology of non-allergic disease states.
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Article: Mast cells in rheumatoid arthritis.Journal of the Royal Society of Medicine 07/1984; 77(6):450-1. · 2.02 Impact Factor
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ABSTRACT: The number and distribution of mast cells were assessed in 116 synovial membranes from patients with rheumatoid arthritis and in 30 control specimens. Rheumatoid synovial membranes contained a mean of 48.5 mast cells per 20 high-power fields (HPF) (range 0-252), and control synovial membranes had a mean of 3.9 mast cells per 20 HPF (range 0-13) (P less than 0.001). In a comparison of high and low mast cell subgroups in rheumatoid arthritis, counts were directly related to the intensity of clinical synovitis in the affected joint, but not to hemoglobin concentration or erythrocyte sedimentation rate. Joints excised from 5 patients with rheumatoid arthritis were characterized by active bone remodeling with increased osteoid, active resorption by osteoclasts, and trabecular osteoporosis. Mast cells were prominent in both extraosseous pannus and intraosseous invasive tissue. The possible roles of mast cells in the pathogenesis of rheumatoid arthritis are discussed.Arthritis & Rheumatology 08/1984; 27(8):845-51. DOI:10.1002/art.1780270802 · 7.87 Impact Factor
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ABSTRACT: Urticaria may develop in response to a number of stimuli such as allergic reactions, drugs, cold, pressure, stings and, most interestingly, neuropsychological upheavals. Classical treatment has utilised H1-receptor antagonists, in view of the fact that histamine released from local mast cells acts on H1-receptors on the vasculature and participates in the pathophysiology of this syndrome. More recently, H2-receptor antagonists have also been tried, alone or in combination, with encouraging results. The question still remains why H2-receptor antagonists should have any beneficial effect since H2-receptors are mostly present on exocrine cells and on T-suppressor lymphocytes, where they are stimulatory, or mast cells, where they are auto-inhibitory. Possible explanations may include the ratio of H1- to H2-receptors on local vasculature and the effect of H2-antagonists on responses elicited through nervous system activity via cholinergic or neuropeptidergic neurons. Finally, evidence is presented that certain tricyclic H-receptor antagonists may have powerful inhibitory effects on secretion from both peripheral and central nervous system mast cells, as well as from neurons. The possible role of H3-receptors in this process is also discussed. At present, the available evidence does not justify the routine use of H2-antagonists in the treatment of urticaria.Drugs 04/1989; 37(3):345-55. DOI:10.2165/00003495-198937030-00004 · 4.13 Impact Factor