TNF- alpha participates in an IgE-mediated cutaneous reaction in mast cell deficient, WBB6F1-W/W super(v) mice

• Published in: Inflammation research Vol. 45; no. 3; pp. 136 - 140
• Main Authors: Nagai, H, Sakurai, T, Abe, T, Matsuo, A, Musoh, K, Tsunematsu, M, Inagaki, N
• Format: Journal Article
• Language: English
• Published: 01-01-1996
• ISSN: 1023-3830

The participation of tumor necrosis factor- alpha (TNF- alpha ) in a IgE-mediated cutaneous reaction in WBB6F1-W/W super(v) (W/W super(v)), 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/W super(v) mice and that prednisolone inhibits the cutaneous reaction at least in part by inhibiting the action of TNF- alpha .