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  • 1
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The α and β forms of recombinant interleukin-1 (IL-1α and IL-1β) and of recombinant Tumor Necrosis Factor (TNFα and TNFβ) induced dose-dependent neutrophil migration into rat peritoneal cavities. Migration induced by both IL-1s showed a bell-shaped dose-response curve and IL-1β was 3-fold more potent than IL-1α. Pretreatment of the animals with dexamethasone or depletion of the peritoneal macrophage population, abolished the neutrophil migration induced by the four cytokines. “In vitro” stimulation of macrophage monolayers with IL-1β and the TNFs released a factor into the supernatant which, unlike these cytokines, induced neutrophil migration in dexamethasone pretreated animals. These results suggest that the neutrophil migration induced by IL-1α, IL-1β and TNFβ is not due to a direct effect on neutrophils, but occurs via the release of a chemotactic factors(s) from resident macrophages.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Inflammation research 24 (1988), S. 377-380 
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Previous experiments of our group have shown that neutrophil migration induced by inflammatory stimuli is reduced by agents which block the release from macrophages of a specific factor for neutrophil migration (MNCF, [1, 2]). The present paper evaluated the influence of macrophage depletion induced by lavage of the peritoneal cavity on neutrophil migration. In both normal and thioglycollatestimuled peritoneal cavities, lavage with saline reduced the resident macrophage population by about 80% and significantly blocked neutrophil migration induced by inflammatory stimuli such as carrageenin, zymosan andE. coli endotoxin. Peritoneal lavage, however, did not affect neutrophil migration induced by MNCF. Thus, these results support the suggestion that macrophages participate in the control of neutrophil migration induced by acute inflammatory stimuli.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Inflammation research 25 (1988), S. 191-194 
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The ability of PAF-acether (platelet activating factor, 1-alkyl-2-acetyl-sn-glycero-3-phosphocholine) to induce neutrophil migration was tested in the peritoneal cavities of rats and guinea-pigs and in rat skin air pouches. PAF-acether, at doses of 2 and 5 μg per animal, did not promote significant neutrophil migration. The ability of PAF-acether antagonists to inhibit carrageenin induced neutrophil migration in rat abdominal cavities was also investigated. Carrageenin is a substance described to cause the release of endogenous PAF-acether. Neutrophil migration was not affected by PAF-antagonists. These observations challenge the possible role of PAF-acether as a neutrophil chemotactic factorin vivo.
    Type of Medium: Electronic Resource
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