title: TNF-alpha participates in an IgE-mediated cutaneous reaction in mast cell deficient, WBB6F1-W/Wv mice.
abstract: 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.
authors.affiliation: Department of Pharmacology, Gifu Pharmaceutical University, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Nagai
authors.forename: T
authors.initials: T
authors.lastname: Sakurai
authors.forename: T
authors.initials: T
authors.lastname: Abe
authors.forename: A
authors.initials: A
authors.lastname: Matsuo
authors.forename: K
authors.initials: K
authors.lastname: Musoh
authors.forename: M
authors.initials: M
authors.lastname: Tsunematsu
authors.forename: N
authors.initials: N
authors.lastname: Inagaki
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage / Q000494:pharmacology*; D000911:Antibodies, Monoclonal / Q000276:immunology; D000918:Antibody Specificity; D004140:Dinitrophenols / Q000276:immunology; D004423:Ear; D004587:Electrophoresis, Agar Gel; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects / Q000235:genetics; D007073:Immunoglobulin E / Q000008:administration & dosage / Q000276:immunology* / Q000378:metabolism; D007274:Injections, Intraperitoneal; D007275:Injections, Intravenous; D051379:Mice; D016133:Polymerase Chain Reaction; D011239:Prednisolone / Q000008:administration & dosage / Q000494:pharmacology*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D011994:Recombinant Proteins / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D012867:Skin / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D013047:Specific Pathogen-Free Organisms; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D014475:Uncoupling Agents / Q000276:immunology
chemical_list: D000893:Anti-Inflammatory Agents; D000911:Antibodies, Monoclonal; D004140:Dinitrophenols; D012333:RNA, Messenger; D011994:Recombinant Proteins; D014409:Tumor Necrosis Factor-alpha; D014475:Uncoupling Agents; D007073:Immunoglobulin E; D011239:Prednisolone