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  • 1
    Electronic Resource
    Electronic Resource
    Agonist-induced calcium flux, phosphoinositide metabolism, aggregation and enzyme secretion in human neutrophils (1988)
    Springer
    Inflammation research 24 (1988), S. 272-282 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Formyl-methionyl-leucyl-phenylalanine (FMLP), platelet activating factor (PAF) and leukotriene B4 (LTB4) are potent activators of human neutrophils. Using human neutrophils prelabelled with the fluorescent indicator dye, Quin 2, or with [32P]-orthophosphate, we examined the effects of these stimuli on intracellular free calcium concentration, [Ca2+]i, and, on various indices of phosphoinositide metabolism, including [32P]-phosphatidic acid (PtdA) formation. The concentration-dependence of the observed changes in [Ca2+]i or [32P]-PtdA were then compared to stimulus-induced aggregation and enzyme release (β-N-acetylglucosaminidase (NAG) and lysozyme). FMLP, PAF and LTB4 caused a concentration-dependent elevation of [Ca2+]i, aggregation and enzyme release. However, unlike FMLP and PAF, LTB4 (≦2.5 μM) did not cause significant formation of [32P]-PtdA. The concentration response curves for agonist-induced elevation of [Ca2+]i lie to the left of those for aggregation and enzyme release. FMLP and PAF also caused an elevation of [Ca2+]i at concentrations lower than those required to elicit [32P]-PtdA formation. These observations suggest that [Ca2+]i elevationper se cannot mediate human neutrophil functional responses to FMLP, PAF and LTB4. Consequently there may exist other mediator(s) that act in concert with [Ca2+]i or are triggered by [Ca2+]i elevation to promote human neutrophil activation. Both the elevation of [Ca2+]i and the formation of these putative mediator(s) in response to LTB4 apparently occur independently of inositol phospholipid hydrolysis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02028283
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Localisation and stimulation of prostacyclin production in vascular cells (1978)
    [s.l.] : Nature Publishing Group
    Nature 271 (1978), S. 549-551 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Pig aortic endothelial cells, aortic medial smooth muscle cells, and aortic adventitial fibroblasts, were isolated and grown in homogeneous monolayer cultures according to previously described methods7'8. For experiments cells were detached (0.1 % trypsin + 0.025% EDTA; 37 C; 2 min) and suspended ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/271549a0
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Effect of prostaglandin E 2 on prostacyclin production by endothelial cells (1979)
    [s.l.] : Nature Publishing Group
    Nature 278 (1979), S. 480-480 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] IT has been suggested by Tomasi et ai1 that prostaglandin (PG) E2 inhibits the synthesis of PGI2 (prostacyclin) by endo-thelial cells. This conclusion was based mainly on their observation that the inhibition of platelet aggregation produced by a suspension of isolated hepatic cells (described as ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/278480a0
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  • 4
    Electronic Resource
    Electronic Resource
    Calcium-dependent stimulation of platelet aggregation by PGE 2 (1975)
    [s.l.] : Nature Publishing Group
    Nature 258 (1975), S. 337-339 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Previous studies of the effects of PGs on platelet aggregation used platelets suspended in citrated plasma (with most of the calcium chelated) or in calcium-free artificial media. The effects of PGEX on several biological systems are influenced by the ionised calcium concentration10'11 and platelet ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/258337a0
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  • 5
    Electronic Resource
    Electronic Resource
    The Effects of IB4, a Monoclonal Antibody to the CD18 Leukocyte Integrin on Phorbol Myristate Acetate (PMA)-Induced Polymorphonuclear Leukocyte (PMN) Accumulation and Endothelial Injury in Rabbit Lungs (1999)
    Springer
    Inflammation 23 (1999), S. 51-62 
    Details
    ISSN: 1573-2576
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A model of acute lung injury induced by intravenous phorbol myristate acetate (PMA) is described. The model is characterized by the accumulation of polymorphonuclear leukocytes (PMNs) and a hemorrhagic edema in bronchoalveolar lavage (BAL) fluid when measured 6 h following the administration of PMA (60 μg/kg, i.v.). It was also determined that PMA induces acute leukopenia and neutropenia which were maximal at 5 min following the injection of PMA and were sustained for at least 6 h, with circulating leukocyte numbers returning to control values by 24 h. The extents to which the inflammatory and systemic changes induced by PMA were dependent on the surface expression on leukocytes of the β2-integrins was assessed by comparing responses to PMA in control animals and animals pretreated with the anti-CD18 monoclonal antibody IB4. The administration of IB4 (1 mg/kg, i.v.) 15 min before PMA did not alter the time course or extent of PMA-induced leukopenia and neutropenia. In contrast IB4 administration (0.1 to 1 mg/kg) produced a dose dependent inhibition of PMN accumulation and plasma extravasation measured in BAL fluid. IB4 (1 mg/kg) completely inhibited PMA evoked increases in plasma extravasation (94.5 ± 1.7%, N = 4) and hemorrhage (95.2 ± 2.1%, N = 4) whereas PMN accumulation in BAL fluid was inhibited by 77.8 ± 3.8% (mean ± SEM, N = 4). Thus, a small, but reproducible, component of the PMA-induced PMN accumulation was not inhibited using this regimen of IB4 administration. If IB4 administration was delayed for 3 h post injection of PMA and bronchoalveolar lavage performed 3 h later, the extents of PMN accumulation and edema formation were similar to those observed 3 h following PMA challenge in control animals not dosed with IB4. This suggests that administration of IB4 during an ongoing inflammatory response is capable of preventing the further development of inflammatory changes and further supports the therapeutic potential of CD18 blockade in conditions such as adult respiratory distress syndrome.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1020239600981
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    Paper (German National Licenses)
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