Trimellitic anhydride (TMA) is widely used industrially to make epoxy and alkyd resins,
plasticizers and
surfactants. The purpose of this study was to investigate whether
contact hypersensitivity (CHS) is induced by repeated TMA challenge and the role of
TNF-alpha and
IgE in the TMA-induced CHS. The repetition of the challenge enlarged the extent of an early and a late phase of CHS in
TNF-alpha+/+ (B6129SF2/J) and Balb/c mice. In the late phase of TMA-induced CHS, the peak of ear swelling responses by single challenge showed at 24 h after challenge, but the peak was observed at 8 h after repeated challenge. In the
TNF-alpha knockout
TNF-alpha-/- (B6;129S-Tnftm1Gk1) mice, the repetition of the TMA challenges enlarged the extent of the late phase of CHS, but less than those in
TNF-alpha+/+ mice. Injection of anti-
TNF-alpha antibody into the peritoneal cavity of Balb/c mice significantly decreased the extent of the late phase of CHS.
Subcutaneous injection of
anti-IgE antibody into Balb/c mice also decreased the extent of the late phase of CHS in dose-dependent manner. Histologically, infiltration of polymorphonuclear leukocytes and eosinophils was more pronounced in repeatedly TMA-challenged
TNF-alpha+/+ and Balb/c mice than in the
TNF-alpha-/- mice and anti-
TNF-alpha or
anti-IgE antibodies treated Balb/c mice. These results indicate that mice sensitized by TMA could possibly offer a useful model to study the mechanism of CHS, and
TNF-alpha and
IgE may act as potential modulators in the late phase of TMA-induced CHS. Neutralization of
TNF-alpha and
IgE by anti-
TNF-alpha or
anti-IgE antibodies may provide therapeutic tools for the treatment of TMA-induced CHS.