Role of chitin in controlling atopic dermatitis (AD)---study on a murine AD model / 中国免疫学杂志

ABSTRACT

Objective:To investigate the effects of chitin on atopic dermatitis in an OVA induced AD murine model.Methods:Twenty-eight BALB/c mice were randomly divided into three groupsthe normal control group (N)(8),the chitin group(E) (10) and the AD model group(M)(10).The murine model of atopic dermatitis was established through intraperitoneal injection of OVA followed by repeated epicutaneous application of OVA on mice back skin( AD model group).During the set up of AD murine model,mice of the chitin group were given intragastric gavage of 3 mg/d for 4 weeks.At the end of the experiment, the mice were sacrificed and skin lesions were biopsied for histological study.HE and O-toluidine stained paraffin sections were observed under microscope.The spleen cells were cultured and challenged with OVA and chitin,respectively,the supernatant was obtained for cytokine determination.Serum levels of total and OVA-specific IgE and total IgG2a were determined with ELISA.Results:Chitin significantly inhibited skin inflammation induced by OVA.Compared with the AD model group,the thickness of the epidermis and dermis in the chitin group were obviously decreased.The numbers of dermal infiltrated inflammatory cells,eosinophils and mast cells were significantly decreased in the chitin group compared with the AD model group ( P<0.05-0.001 ).The serum level of total IgE and OVA-specific IgE were significantly lower in the chitin group than in the AD model group(P<0.05-0.001),while the serum level of IgG2a in the chitin group was significantly higher than that of the AD model group( P<0.001).The cultured spleen cells of the chitin group produced significantly higher levels of IL-12 and IFN-γ,but lower level of IL-4 compared with those of the AD model group after OVA challenge (P<0.05).Conclusion:Chitin can inhibit the inflammation and decease the seum level of IgE in the murine AD model.The antiallergic effect of chitin might be associated with the induced production of Th1 type cytokines by mice spleen cells.