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  • 1
    Electronic Resource
    Electronic Resource
    The effect of receptor-mediated stimulation on the translocation of 5-lipoxygenase (1994)
    Springer
    Inflammation research 41 (1994), S. C169 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract It has been shown that calcium ionophore-mediated activation of the 5-lipoxygenase is followed by an extensive loss of enzyme activity. We investigated whether IgE/antigen stimulation of mast cells leads to a similar inactivation. This challenge caused a minor loss of 5-lipoxygenase activity as compared to A23187. Both stimuli resulted in the synthesis of similar amounts of leukotrienes. Immunoblot experiments showed that after antigen, the membrane association of the enzyme was reversible. In contrast, with A23187 translocation continued during the time of observation (60 min). Calcium chelators, added after A23187 stimulation, stopped the enzyme inactivation and reversed the membrane binding. The data suggest that the continuous, high intracellular calcium levels initiated by A23187 inactivate the enzyme, while the transient increase in calcium during receptor-mediated stimulation is sufficient to activate the 5-lipoxygenase but not to extensively inactivate it.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01987625
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  • 2
    Electronic Resource
    Electronic Resource
    Mast cell modulation of immune responses to bacteria (2001)
    Copenhagen : Munksgaard International Publishers
    Immunological reviews 179 (2001), S. 0 
    Details
    ISSN: 1600-065X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Summary: Mast cells are key elements of the immune system. These cells release a wide variety of pro-inflammatory mediators which are responsible for the pathophysiology of many allergic diseases. Recent studies, however, have shown that mast cells have the capacity to modulate the host's innate immune response to gram negative bacteria by their ability to phagocytose bacteria, process and present bacterial antigens to T cells and recruit phagocytic help through the release of physiological amounts of pro-inflammatory mediators. Here, current knowledge of mast cell responses to gram negative bacteria and molecular mechanisms associated with mast cell bacteria interaction is reviewed.This work was supported in part by NIH research grant AI45013. We are grateful to Ms. Tamara Paul for critical review of the manuscript.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1034/j.1600-065X.2001.790102.x
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  • 3
    Electronic Resource
    Electronic Resource
    Survival of FimH-expressing enterobacteria in macrophages relies on glycolipid traffic (1997)
    [s.l.] : Macmillan Magazines Ltd.
    Nature 389 (1997), S. 636-639 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Strains of Escherichia coli persist within the human gut as normal commensals, but are frequent pathogens and can cause recurrent infection. Here we show that, in contrast to E. coli subjected to opsonic interactions stimulated by the host's immune response, E.coli that bind to the macrophage ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/39376
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  • 4
    Electronic Resource
    Electronic Resource
    Mast cell modulation of neutrophil influx and bacterial clearance at sites of infection through TNF-α (1996)
    [s.l.] : Nature Publishing Group
    Nature 381 (1996), S. 77-80 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] A mouse-virulent strain of Klebsiella pneumoniae, KPA1, was injected into the peritoneal cavities of 4/4 and W/WV mice. After 48 h, the number of bacteria surviving in the peritoneal cavities of W/WV mice was about 20-fold higher than in 4/4 mice (Fig. la). Apparently, the mast-cell- deficiency ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/381077a0
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  • 5
    Electronic Resource
    Electronic Resource
    Pharmacokinetics and Biologic Activity of the Novel Mast Cell Inhibitor, 4-(3′-Hydroxyphenyl)-amino-6,7-dimethoxyquinazoline in Mice (1999)
    Springer
    Pharmaceutical research 16 (1999), S. 117-122 
    Details
    ISSN: 1573-904X
    Keywords: WHI-P180 ; pharmacokinetics ; quinazolines ; mast cell inhibitor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Abstract Purpose. The purpose of the present study was to examine the pharma-codynamic and pharmacokinetic features of the novel mast cell inhibitor 4-(3′-Hydroxyphenyl)-amino-6,7-dimethoxyquinazoline (WHI-P180) in mice. Methods. A high performance liquid chromatography (HPLC)-based quantitative detection method was used to measure plasma WHI-P180 levels in mice. The plasma concentration-time data was fit to a single compartment pharmacokinetic model by using the WinNonlin program to calculate the pharmacokinetic parameters. A cutaneous anaphylaxis model was used to examine the pharmacodynamic effects of WHI-P180 on anaphylaxis-associated vascular hyperpermeability. Results. The elimination half-life of WHI-P180 in CD-1 mice (BALB/ c mice) following i.v., i.p., or p.o. administration was less than 10 min. Systemic clearance of WHI-P180 was 6742 mL/h/kg in CD-1 mice and 8188 mL/h/kg in BALB/c mice. Notably, WHI-P180, when administered in two consecutive nontoxic i.p. bolus doses of 25 mg/kg, inhibited IgE/antigen-induced vascular hyperpermeability in a well-characterized murine model of passive cutaneous anaphylaxis. Conclusions. WHI-P180 is an active inhibitor of IgE-mediated mast cell responses in vitro and in vivo. Further preclinical characterization of WHI-P180 may improve the efficacy of WHI-P180 in vivo and provide the basis for design of effective treatment and prevention programs for mast cell mediated allergic reactions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1018835232027
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    Paper (German National Licenses)
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