ABSTRACT
Objective To construct a recombinant adenovirus vector expressing mouse SPINK5 gene,and observe its curative effect on the skin lesions in atopic dermatitis mice model. Methods By recombining DNA technology,the sequence of mouse SPINK5 gene was cloned into adeno?virus shuttle plasmid. Then it was transformed into HEK 293 cells with the adenoviral backbone plasmid to obtain the recombinant adenovirus. A mouse model of atopic dermatitis was established by system and local sensitization of Balb/c mice with ovalbumin . The effect of recombinant adeno?virus on the lesions of atopic dermatitis mice model was observed. Results The SPINK5 over?expressing adenovirus vector and atopic dermatitis mice model were successfully constructed. After 2 weeks of adenovirus?mediated SPINK5 gene intracutaneous injection,the redness and edema of lesions of AD model mice were obvious relieved. The pathological detection indicated that epidermal thickness and prickle cell layer ,inflammatory cell infiltration significant decreased accompanied with the model blank control. Conclusion The adenovirus?mediated SPINK5 gene had signifi?cant therapeutic effect to the atopic dermatitis mice model ,which provided a laboratory basis of application of SPINK5 gene product to therapy atopic dermatitis.
ABSTRACT
Objective To assess the changes in frequency of peripheral T lymphocytes expressing different cytokines in patients with atopic dermatitis (AD) before and after treatment with BCG-PSN and their relationship with disease severity. Methods A randomized, double blinded and placebo cross-over control study was conducted. A total of 8 patients with AD were recruited in this study. Intramuscular BCG-PSN or placebo was given to patients every other day for 36 days. Flow cytometry was performed to measure the frequency of IL4-, IL5-, IFN-γ- and TNFα-expressing peripheral CD4+ T cells and CD8+ T cells before and after the therapy. Disease severity was evaluated by atopic dermatitis area and severity index score (ADASIS). Results The difference value in IFN-γ+CD8+ T cell frequency before and after therapy was significantly higher in patients treated with BCG-PSN than in those with placebo (8.056 ± 13.962 vs -6.549 ± 10.491, U = 2.26, P< 0.05). There was no statistical difference in the frequency of IL4-, IL5-, TNFa-expressing CD8+ T cells between BCG-PSN- and placebo-treated patients (all P > 0.05). The decrease in ADASIS was 1.56 ± 1.49 in patients treated with BCG-PSN, which was statistically higher than that in placebo-treated patients (-0.05 ± 1.54, U = 2.00, P< 0.05). Conclusion As an immunomodulator, BCG-PSN may control AD by restoring the balance of T-cell subsets.