Protective effect of polysaccharide nucleic acid fraction of bacillus Calmette-Guerin against atopic dermatitis in Nc/Nga mice

2015 
Objective To evaluate the protective effect of polysaccharide nucleic acid fraction of bacillus Calmette-Guerin (BCG-PSN) against atopic dermatitis (AD) in Nc/Nga mice, and to explore its possible mechanism. Methods Sixteen Nc/Nga mice were classified into normal control group (n = 4) , low-concentration BCG-PSN group (n=5) and high-concentration BCG-PSN group (n=7) to be subcutaneously injected with sodium chloride physiological solution, BCG-PSN of 0.1 mg/kg and 0.5 mg/kg respectively, at 1, 8, 15 and 22 days of age. Dinitrochlorobenzene (DNCB) was repeatedly and topically applied to these Nc/Nga mice to induce AD-like lesions at 49 days of age. The preventive effect of BCG-PSN against AD was evaluated by dermatitis scores, scratching frequency, histopathological manifestations and immunological parameters (including IgE, interleukin (IL) -4 and -12, and interferon (IFN) -γ) . Results Repeated injection of BCG-PSN within 4 weeks after birth significantly decreased the severity of DNCB-induced AD-like lesions, dermatitis scores and scratching behavior in Nc/Nga mice. There was no statistical difference in scratching frequency between the high- and low-concentration BCG-PSN groups. BCG-PSN treatment reduced the plasma level of IgE in Nc/Nga mice in a dose-dependent manner. BCG-PSN at 0.5 mg/kg increased the number of cells secreting IFN-γ in skin lesions of mice. Both doses of BCG-PSN down-regulated IL-4 level, but up-regulated IL-12 level in the culture supernatant of spleen mononuclear cells from mice. Conclusion Early injection of BCG-PSN could protect Nc/Nga mice against dermatitis by promoting the proliferation of IFN-γ-secreting cells, increasing the synthesis of IL-12, and reducing the levels of IL-4 and IgE. Key words: Dermatitis, atopic; Mice, Nc/Nga; Dendritic cells; BCG-PSN
    • Correction
    • Source
    • Cite
    • Save
    • Machine Reading By IdeaReader
    0
    References
    0
    Citations
    NaN
    KQI
    []