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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 629 (1991), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Springer seminars in immunopathology 12 (1990), S. 415-428 
    ISSN: 1432-2196
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The duration and severity of the allergic response are variable. Even though antigens are rapidly cleared from the individual, an acute allergic response is frequently followed by a recrudescence of symptoms hours or even days after the initial exposure. Experimentally, the cellular infiltrates and mediators released during this late response resemble those associated with chronic inflammatory disease. Although basophils are present in this late reaction, the stimuli for their activation remain unknown. A heterogeneous group of unique cytokines called histamine-releasing factors (HRF), discovered over a decade ago, may well play a role in stimulating basophils during this late-phase reaction. These factors have been reported from a variety of cell sources including alveolar macrophages, platelets, vascular endothelial cells, B and T lymphocytes, mononuclear cell cultures, the U937 monocyte/macrophage-like cell line and the RPMI 8866 B cell line. These ubiquitous factors cause non-cytotoxic, calcium-dependent mediator release from human basophils in vitro and are also present and active in vivo. Purification attempts have revealed that HRF exists in at least three forms, based on molecular weight. In our hands, the mechanism of mediator release by one of the forms of HRF is IgE dependent. Since only about 50% of allergic donors' basophils respond to HRF, a heretofore unappreciated heterogeneity of IgE was revealed. The presence of HRF has been shown to correlate with severity of allergic disease in children with food allergies, with symptoms in the late-phase response in adults and with severity of the allergic response to an inhaled antigen. Thus, the study of HRF has evolved over the last decade and may lead to better understanding of the complex allergic response.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Digestive diseases and sciences 36 (1991), S. 179-184 
    ISSN: 1573-2568
    Keywords: intestinal mast cells ; basophils ; histamine ; prostaglandin D2 ; sulfasalazine ; 5-aminosalicylic acid
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Intestinal mast cells are thought to contribute to the mucosal inflammation in ulcerative colitis and Crohn's disease through release of inflammatory mediators. Since sulfasalazine and its metabolite 5-aminosalicylic acid are effective therapeutic agents in inflammatory bowel disease and have been shown to inhibit generation of inflammatory products in other cells, we examined the effect of these agentsin vitro on human intestinal mast cell mediator release. Sulfasalazine (5×10−4−10 −3 M) was found to significantly enhance goat anti-human IgE-induced histamine release from intestinal mast cells, which is the same response as seen in human blood basophils, whereas its metabolite 5-aminosalicylic acid was an effective inhibitor of stimulated histamine release in both mast cells and basophils. 5-Aminosalicylic acid also inhibited production of prostaglandin D2 by the stimulated intestinal mast cells. Sulfasalazine alone, without immunologic stimulation, did not induce histamine release from mast cells or basophils, but the enhancement of ongoing mast cell activation by sulfasalazine may explain some cases of adverse reactions to the drug. The inhibition of mast cell histamine release and prostaglandin generation by 5-aminosalicylic acid demonstrates a potential therapeutic modality of this agent.
    Type of Medium: Electronic Resource
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