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  • 1
    Electronic Resource
    Electronic Resource
    Reduced Natural Killer Cell Activity in Multi-Drug Resistant Pulmonary Tuberculosis (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 36 (1992), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Cellular immune status in five patients with multi-drug resistant pulmonary tuberculosis was investigated and compared with five matched controls with non-resistant tuberculosis. A significant reduction in fresh natural killer (NK)-cell activity was found in the resistant group (P 〈 0.005). There were no significant differences between the two groups in lymphocyte phenotype, proliferation or PPD-specific cytotoxicity. Reduced NK-cell function may play a role in the pathogenesis of multi-drug resistant pulmonary tuberculosis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-3083.1992.tb01643.x
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    A Biological Role for Ascorbate in the Selective Neutralization of Extracellular Phagocyte-derived Oxidants (1987)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 498 (1987), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1987.tb23764.x
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  • 3
    Electronic Resource
    Electronic Resource
    Benoxaprofen: A pro-oxidant anti-inflammatory drug? (1984)
    Springer
    Inflammation research 14 (1984), S. 238-246 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Benoxaprofen inhibited the random motility and migration to the leucoattractants endotoxin-activated serum (EAS) and f-met-leu-phe of human polymorphonuclear leucocytes (PMNL)in vitro. Inhibition of random and leucoattractant-induced migration was observed at drug concentrations of 〉1×110−6 M and 1×10−5 M respectively. Benoxaprofenper se was not leucotactic but was pro-oxidative in that it stimulated PMNL hexose-monophosphate shunt activity, chemiluminescence, myeloperoxidase-mediated iodination reactions and degranulation. The drug also mediated auto-oxidation of PMNL as measured by cellular auto-lodination. The relationship between benoxaprofen-mediated inhibition of PMNL migration and activation of oxidative metabolism was investigated using the anti-oxidants ascorbate and levamisole at concentrations of 10−2 M and 10−3 M respectively. These agents prevented the decreased motility and auto-oxidation of PMNL induced by 10−4 M benoxaprofen. Benoxaprofen (10−4 M) did not inhibit the migration of PMNL from 3 children with chronic granulomatous disease thus showing that intact PMNL oxidative metabolism is required for the induction of drug-mediated inhibition of cell motility. Ingestion of therapeutic doses of benoxaprofen for 7 days by normal adults gave serum drug concentrations greater than those required for detectable effects on PMNL functionsin vitro (mean serum value 126 μg/ml). Co-incubation of normal PMNL with serum from individuals who had ingested the drug caused decreased cell migration and increased chemiluminescence. These results show that benoxaprofen inhibits PMNL migration as a consequence of pro-oxidant properties and despite its withdrawal may be the prototype of the pro-oxidative anti-inflammatory drug.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01966648
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  • 4
    Electronic Resource
    Electronic Resource
    Effects of benoxaprofen on the binding to and inactivation of leucoattractants by human polymorphonuclear leucocytesin vitro (1985)
    Springer
    Inflammation research 16 (1985), S. 527-534 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Benoxaprofen was previously found to inhibit the random and leucoattractant-induced migration of human polymorphonuclear leucocytesin vitro by a pro-oxidative mechanism [1]. In this study the effects of benoxaprofen on the binding to PMNL of the synthetic chemotactic tripeptide FMLP, on the oxidative inactivation of this leucoattractant by PMNL and on PMNL chemotaxis, chemokinesis and orientation in an FMLP gradient have been investigated. At concentrations of 10−5 M (3 μg/ml) benoxaprofen inhibited PMNL random and leucoattractant-induced migration and increased PMNL membraneassociated oxidative metabolism and cellular auto-oxidation. These effects of benoxaprofen on PMNL migration and auto-oxidation were prevented by the anti-oxidant cysteine (10−3 M). Benoxaprofen inhibited both FMLP-induced chemotaxis and chemokinesis but did not affect the binding of radiolabelled FMLP to PMNL or orientation of the cells in a positive gradient of the leucoattractant. Benoxaprofen at concentrations of 5×10−5 M significantly increased the oxidative inactivation of FMLP by PMNL. Inhibition of PMNL migration by benoxaprofen is mediated by the two different pro-oxidative mechanisms, viz. a cell-directed auto-oxidative mechanism and potentiation of the oxidative inactivation of leucoattractants by PMNL.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01983658
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    Paper (German National Licenses)
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