TNF-α 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.

Inhibitory Effect of Dietary Carotenoids on Dinitrofluorobenzene-Induced Contact Hypersensitivity in Mice

“…This second response is dependent on such inflammatory cytokines as TNFand IL-1 that are secreted from mast cells and macrophages. [7][8][9] These results indicate that mast cells play a pivotal role in the contact hypersensitivity induced by DNFB.…”

Possible Role of Nitric Oxide in IgE-Mediated Allergic Cutaneous Reaction in Mice

“…IgE-mediated biphasic cutaneous reactions were evoked in BALB/c mice as reported previously [16, 17, 18, 19]. Briefly, mice were passively sensitized by an intravenous injection of 1.0 ml monoclonal IgE preparation.…”

“…Mouse monoclonal IgE against DNP residue was prepared by culturing a cell line, EC1, as reported previously [16, 17, 18]. The culture supernatant of EC1 was used as a source of IgE.…”

“…data]. We also indicated the participation of proinflammatory cytokines, such as interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α), especially in the late phase [18, 19]. These cytokines could cause ear edema directly, which may correspond to the late phase.…”

“…The immediate-phase edema is characterized by a rapid increase in capillary permeability caused by mast cell mediators, whereas the late-phase edema is characterized by recruitment of inflammatory cells such as neutrophils, macrophages and eosinophils [17, 18]. In addition, the biphasic cutaneous reaction is also characterized by marked vascular dilatation, especially in its late phase [unpubl.…”