The participation of tumor necrosis factor-alpha (TNF-alpha) 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 48-72 h after the antigen challenge. A monoclonal anti-tumor necrosis factor (TNF)-alpha antibody inhibited the IgE-mediated cutaneous reaction. An increase of TNF-alpha mRNA was demonstrated 4 h after the application of antigen by the reverse transcriptase-polymerase chain reaction. The injection of recombinant murine TNF-alpha 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-alpha-mRNA. Prednisolone at doses of 1 to 10 mg/kg clearly inhibited the TNF-alpha-induced cutaneous reaction. These results suggest that TNF-alpha 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-alpha.
The effects of IFN-β and prednisolone (Pred) on antigen-induced IgE antibody production, airway eosinophilia and airway hyperreactivity (AHR) were studied in ovalbumin-sensitized Balb/c mice. Three inhalations of antigen (ovalbumin) caused an increase in the number of eosinophils and lymphocytes in bronchoalveolar lavage fluid and AHR to acetylcholine with a significant elevation in the serum IgE level. IFN-β clearly inhibited the antigen-induced airway inflammation and AHR, but did not affect IgE antibody production. Pred inhibited antigen-induced IgE antibody production, airway inflammation and AHR to acetylcholine. In addition, IFN-β inhibited T-helper type 2 (Th2) cell clone (D10G4.1)-induced peritoneal eosinophilia in mice, but did not affect neutrophilia, whereas Pred inhibited D10G4.1-induced peritoneal eosinophilia and neutrophilia. These results suggest that IFN-β inhibits antigen-induced bronchial inflammation and AHR probably due to the inhibition of Th2-induced airway eosinophilia.
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