Hsu C H, Chua K Y, Huang S K, Chiang I P, Hsieh K H
Graduate Institutes of Microbiology and Immunology, National Taiwan University, Taipei, Republic of China.
Clin Exp Allergy. 1996 Nov;26(11):1329-37.
The molecular and functional basis of allergen-induced inflammation seen in atopic dermatitis (AD) remains undefined.
The objective of this study is to establish a murine model to dissect the pathological mechanisms of inflammatory reactions leading to the development of AD.
An inbred strain of mice, BALB/c, when injected peritoneally with 30 micrograms of recombinant Sj26 protein (rSj26), a glutathione-S-transferase of Schistosoma japonicum worm, developed systematic dermatitis 21 days after immunization. The pathology of the dermatitis was examined by histological evaluation and immunostaining. The immediate skin hypersensitivity was demonstrated by serum transfer and skin test. Epicutaneous patch test was used to demonstrate the antigen-specific late phase response.
Significant responses of rSj26-specific IgE were detected 2 weeks after immunization, and such changes paralleled formation of skin lesions. The diseased skin pathology showed inflammatory changes such as infiltration of mononuclear cells and eosinophils in the dermis and mild spongiosis in the epidermis. Numerous IgE bearing cells were also detected in the dermis. Peripheral blood showed eosinophilia at the same time. In addition, rSj26-specific positive skin test and epicutaneous patch test could be demonstrated in rSj26-sensitized mice.
These results suggest that rSj26 is capable of eliciting atopic dermatitis-like lesions in BALB/c mice. This can be a useful animal model for elucidating allergen-induced immune responses and the development of various therapeutic interventions of atopic dermatitis in humans.
