Nagai H, Sakurai T, Abe T, Matsuo A, Musoh K, Tsunematsu M, Inagaki N
Department of Pharmacology, Gifu Pharmaceutical University, Japan.
Inflamm Res. 1996 Mar;45(3):136-40. doi: 10.1007/BF02265167.
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.
研究了肿瘤坏死因子-α(TNF-α)在WBB6F1-W/Wv(W/Wv)肥大细胞缺陷小鼠的IgE介导的皮肤反应中的作用以及泼尼松龙对该皮肤反应的影响。通过静脉注射单克隆抗二硝基苯酚(DNP)IgE使小鼠被动致敏,24小时后用二硝基氟苯对其耳部进行表皮攻击。通过耳部厚度评估的皮肤反应在抗原攻击后48-72小时达到峰值。单克隆抗肿瘤坏死因子(TNF)-α抗体抑制了IgE介导的皮肤反应。通过逆转录聚合酶链反应证明在应用抗原后4小时TNF-α mRNA增加。注射重组小鼠TNF-α在未致敏小鼠中诱导出皮肤反应,该反应在24小时达到峰值。剂量为3至10mg/kg的泼尼松龙明显抑制了IgE介导的皮肤反应,然而,它不影响TNF-α mRNA的表达。剂量为1至10mg/kg的泼尼松龙明显抑制了TNF-α诱导的皮肤反应。这些结果表明TNF-α在W/Wv小鼠的IgE介导的皮肤反应中起作用,并且泼尼松龙至少部分地通过抑制TNF-α的作用来抑制皮肤反应。