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  • 1
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Natural killer (NK) cells may provide the basis for resistance to Trypanosoma cruzi infection, because the depletion of NK1.1 cells causes high levels of parasitemia in young C57Bl/6 mice infected with T. cruzi. Indeed, NK1.1 cells have been implicated in the early production of large amounts of interferon (IFN)-γ, an important cytokine in host resistance. The NK1.1 marker is also expressed on special subpopulations of T cells. Most NK1.1+ T cells are of thymic origin, and their constant generation may be prevented by thymectomy. This procedure, by itself, decreased parasitemia and increased resistance in young mice. However, the depletion of NK1.1+ cells by the chronic administration of a monoclonal antibody (MoAb) (PK-136) did not increase the parasitemia or mortality in thymectomized C57Bl/6 mice infected with T. cruzi (Tulahuen strain). To study the cross-talk between NK1.1+ cells and conventional T cells in this model, we examined the expression of activation/memory markers (CD45RB) on splenic CD4+ and CD8+ T cells from young euthymic or thymectomized mice with or without depletion of NK1.1+ cells and also in aged mice during acute infection. Resistance to infection correlated with the amount of CD4+ T cells that are already activated at the moment of infection, as judged by the number of splenic CD4+ T cells expressing CD45RB−. In addition, the specific antibody response to T. cruzi antigens was precocious and an accumulation of immunoglobulin (Ig)M with little isotype switch occurred in euthymic mice depleted of NK1.1+ cells. The data presented here suggest that NK1.1+ cells have important regulatory functions in euthymic, but not in thymectomized mice infected with T. cruzi. These regulatory functions include a helper activity in the generation of effector or activated/memory T cells.
    Type of Medium: Electronic Resource
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  • 2
    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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  • 3
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We have previously reported that rat peritoneal macrophages stimulated with LPS release a factor (MNCF) which induces neutrophil migration that is not blocked by glucocorticoids. The supernatant of macrophage monolayers stimulated with LPS was submitted to affinity chromatography on immobilized sugar columns. We observed that thed-gal binding fraction retained MNCF activity. This fraction, consisting of four protein components, was submitted to chromatography on Superdex 75, yielding a homogeneous preparation of the active component. MNCF has a MW of 54 KDa (gel filtration and SDS-PAGE) and pI〈4.0 (isoelectrofocusing and chromatofocusing).d-gal did not interfere with the behaviour of known interleukins (IL-1β, IL-6, IL-8 TNF-α), but blocked MNCF activity in anin vitro migration assay. The present results reinforce our previous suggestion that MNCF may correspond to a novel monokine which induces neutrophil migration through a direct mechanism involving thed-gal binding site of the molecule.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Using specific antisera for IL-1β and IL-8, as well as cyclooxygenase inhibitors and propranolol, we have demonstrated that these cytokines are responsible for the prostaglandin and sympathetic components of carrageenin-induced hyperalgesia in the rat paw test. The release of IL-1β and IL-8 is preceded by the liberation of TNF-α. We have also tested in a nociceptive model the effects of bradykinin and a specific bradykinin antagonist, HOE 140, on the hyperalgesia induced by carrageenin and lipopolysaccharide (LPS). Bradykinin-induced hyperalgesia was abolished by HOE 140 and by treatment of the paws with anti-TNF-α antisera. HOE 140 significantly inhibited the hyperalgesia induced by carrageenin and LPS. It is suggested that in these two models bradykinin is associated with the release of hyperalgesic cytokines.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Mice inoculated withPlasmodium berghei developed a drastic and significant pulmonary edema. Treatment of animals with phenoxybenzamine rendered mice hyporeactive to this physiopathological alteration.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 7
    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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  • 8
    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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  • 9
    ISSN: 1573-2576
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Canatoxin (Cntx), a toxic protein purified fromCanavalia ensiformis seeds, was shown to have lipoxygenase-mediated effects either in vivo or in vitro. Data here show that Cntx induced a dose-dependent migration of neutrophils and mononuclear cells when injected into rat peritoneal cavities. Furthermore, Cntx was able to induce neutrophil migration into pleural cavities and into air pouches. These effects were inhibited by dexamethasone but not by inhibitors of arachidonic acid metabolism (indomethacin, NDGA, and BW-755c) or by a PAF antagonist (BN 52021). In the peritoneal cavity Cntx caused an increase in vascular permeability inhibited by dexamethasone and BW-755c. Neutrophil migration induced by this toxin was dependent on the number of resident macrophages, since the migratory effect was enhanced by increasing the peritoneal macrophage population with thioglycollate pretreatmen; and was diminished when this population was reduced by peritoneal wash. It was also observed that Cntx induced release of a chemotactic factor from macrophage monolayers in vitro. Dexamethasone blocked this release but did not affect in vivo neutrophil recruitment induced by that factor. These data suggest that Cntx-induced neutrophil migration may be mediated by the same macrophage-derived neutrophil chemotactic factor released by other stimuli such as LPS, IL-1, and INF-gamma.
    Type of Medium: Electronic Resource
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