This experiment pursued the time course of contact hypersensitivity to 2,4-dinitro-1-fluorobenzene (DNFB) and histologic changes of the cutaneous reaction in mice. The contact hypersensitivity reached a maximum 4 days after sensitization (96.9 +/- 6.7% vs. 22.7 +/- 1.3% in control) and persisted for 3 weeks. The cutaneous hypersensitivity reaction showed peak reactivity at 24 hr after challenge (96.2 +/- 4.7% vs. 11.5 +/- 1.7% in control), and persisted up to 96 hr (13.2 +/- 2.1%). Prime histologic changes observed in this experiment were the exocytosis of lymphoid cells and epidermal thickening which appeared at 20 hr after challenge. Edema, vasodilatation and increased mast cells were observed within the dermis at 4-8 hr. However, edema and vasodilatation disappeared gradually, but numbers of mast cell increased up to 96 hr. The dermal infiltrates were maximum at the 28-72 hr after challenge.
Animals ; Dermatitis, Contact/immunology/*pathology ; Dinitrofluorobenzene/*pharmacology ; Ear ; Female ; Mice ; Mice, Inbred BALB C ; Nitrobenzenes/*pharmacology ; Time Factors

This study is to observe the inhibition of etoposide on allergic contact dermatitis (ACD) and explore its possible mechanism of action. Dinitrofluorobenzene was used to induce the allergic contact dermatitis in mouse ear. Three groups of animals were orally administrated with different doses of VP-16 (5, 10, and 20 mg x kg(-1)), separately, for six days. The degree of skin inflammatory reaction was observed by optical microscope. Expression of intercellular adhesion molecule (ICAM-1) was detected by immunohistochemical staining. Radioimmunoassay was applied to measure the serum level of tumor necrosis factor-alpha (TNF-alpha) and interleukin-10 (IL-10). VP-16 significantly decreased inflammatory cell infiltration and the degree of infiltration reaction, and decreased the level of TNF-a in serum and the expression of ICAM-l in skin. VP-16 can significantly inhibit allergic contact dermatitis induced by DNFB. This therapeutic effect of VP-16 on murine ACD may be due to inhibiting expression of some cytokines.
Animals ; Anti-Inflammatory Agents ; pharmacology ; Dermatitis, Allergic Contact ; blood ; etiology ; metabolism ; Dinitrofluorobenzene ; Etoposide ; pharmacology ; Female ; Intercellular Adhesion Molecule-1 ; metabolism ; Interleukin-10 ; blood ; Male ; Mice ; Random Allocation ; Skin ; metabolism ; Tumor Necrosis Factor-alpha ; blood