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  • IgE  (2)
  • Allergic cutaneous reaction  (1)
  • Collagen-induced arthritis  (1)
  • 1
    ISSN: 1420-908X
    Keywords: Allergic cutaneous reaction ; IgE ; TNF-α ; Glucocorticoid ; WBB6F1-W/Wv mice
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The participation of tumor necrosis factor-α (TNF-α) in a IgE-mediated cutaneous reaction in WBB6F1-W/Wv (W/Wv), mast cell deficient, mice and the effect of prednisolone on this cutaneous reaction were investigated. Mice were passively sensitized by an intravenous injection of monoclonal anti-dinitrophenol (DNP) IgE, and their ears challenged epicutaneously with dinitrofluorobenzene 24 h later. The cutaneous reaction estimated by ear thickness reached a peak 48–72h after the antigen challenge. A monoclonal anti-tumor necrosis factor (TNF)-α antibody inhibited the IgE-mediated cutaneous reaction. An increase of TNF-α mRNA was demonstrated 4h after the application of antigen by the reverse transcriptase-polymerase chain reaction. The injection of recombinant murine TNF-α induced a cutaneous reaction which peaked at 24 h in nonsensitized mice. Prednisolone at doses of 3 to 10 mg/kg clearly inhibited the IgE-mediated cutaneous reaction, however, it did not affect the expression of TNF-α-mRNA. Prednisolone at doses of 1 to 10 mg/kg clearly inhibited the TNF-α-induced cutaneous reaction. These results suggest that TNF-α plays a role in the IgE-mediated cutaneous reaction in W/Wv mice and that prednisolone inhibits the cutaneous reaction at least in part by inhibiting the action of TNF-α.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1420-908X
    Keywords: Rat peritoneal mast cell ; Rat peritoneal non-mast cell ; IgE ; Histamine release ; Regulation of histamine release
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Histamine release from purified rat peritoneal mast cells (PMC) was examined and compared to that from a non-purified preparation (PEC). Both PEC and PMC released similar amounts of histamine upon stimulation with compound 48/80, calcium ionophore A23187 and substance P. In contrast, IgE-dependent histamine release from PMC caused by antigen, anti-IgE and concanavalin A was very low compared to that of PEC. The reduced IgE-dependent histamine release from PMC, however, was recovered when PMC was reconstituted with non-mast cells (NMC) present in the peritoneal cavity. The effect was time-dependent and reached a plateau in 30 min. NMC from both sensitized and non-sensitized rats recovered the reduced histamine release from PMC dose-dependently. The potentiating effect of NMC was observed even in the presence of excess amount of phosphatidylserine. Supernatants of NMC and a mixture of PMC and NMC incubated for 1 hr at 37°C, however, failed to potentiate the histamine release. These results demonstrate that IgE-dependent histamine release from rat peritoneal mast cells is upregulated by other cells present in the peritoneal cavity, and that the mechanism involved is distinct from that of phosphatidylserine.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Inflammation research 45 (1996), S. 293-298 
    ISSN: 1420-908X
    Keywords: Mesoporphyrin ; T cell ; Collagen-induced arthritis ; Superantigen
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of mesoporphyrin, a novel porphyrin derivative, on type II collagen-induced arthritis in mice were studied. Mesoporphyrin (10–30 mg/kg) and prednisolone (5 mg/kg; reference drug) reduced the incidence and severity of type II collagen-induced arthritis in mice, as assayed by clinical observation and histopathological studies. Although both agents inhibited type II collagen-induced delayed type hypersensitivity in arthritic mice, only prednisolone inhibited humoral immunity to type II collagen. The effects of mesoporphyrin on T cell dependent allergic inflammation were examined, in order to study the mechanism by which it inhibits arthritis. Staphylococcal enterotoxin B (SEB; superantigen)-potentiated collagen-induced arthritis and sheep red blood cell-induced delayed type hypersensitivity reaction were clearly inhibited by mesoporphyrin. Moreover, the superantigen-induced CD-25 expression on T cells was inhibited by mesoporphyrin. These results indicate that mesoporphyrin inhibits type II collagen-induced arthritis by inhibiting the activation of T cells.
    Type of Medium: Electronic Resource
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