Effects of TNCB sensitization in DS-Nh mice, serving as a model of atopic dermatitis, in comparison with NC/Nga mice.
BACKGROUND
It has been predicted that a type-1 and type-2 helper T cell (Th1/Th2) imbalance exists in atopic dermatitis (AD). In DS-Nh mice, an AD mouse model, Staphylococcus aureus increases on the skin surface.


OBJECTIVE
To investigate whether the Th1-dominant response has an influence on the development of AD, we induced chronic allergic hypersensitivity with 2,4,6-trinitrochlorobenzene (TNCB ) in two AD mouse models: NC/Nga mice and DS-Nh mice. Th1 and Th2 cytokine production of splenocytes was assessed under stimulation with staphylococcal enterotoxin B (SEB) which induces a Th1 response in DS-Nh mice with or without TNCB sensitization.


METHODS
We examined clinical skin changes, transepidermal water loss (TEWL), the number of S. aureus on the skin and the serum IgE levels in these mice treated repeatedly with TNCB under conventional conditions (free of fur mites). The splenocytes of DS-Nh mice were cultured with SEB and the cytokine levels in the supernatants were measured by enzyme-linked immunosorbent assay (ELISA).


RESULTS
Significant skin changes were observed on the skin even where TNCB was not applied in both mice treated with TNCB. Increases in S. aureus on the skin and serum IgE levels were detected in DS-Nh mice, but not in NC/Nga mice. In DS-Nh mice, IFN-gamma and IL-13 production of splenocytes increased in the mice treated with TNCB.


CONCLUSIONS
These results suggest that there might be a different mechanism of dermatitis induction between NC/Nga and DS-Nh mice. Th1 responses might play an important role in the development of dermatitis and increase in serum IgE levels in DS-Nh mice through an increase in IL-13 production.
Matsukura
Setsuko
S
Department of Environmental Immuno-Dermatology, Yokohama City University Graduate School of Medicine, Yokohama, Japan. s.matsukura@aa.bb-east.ne.jp
Aihara
Michiko
M
Hirasawa
Tsutomu
T
Ikezawa
Zenro
Z
D000818:Animals; D016207:Cytokines / Q000276:immunology; D003876:Dermatitis, Atopic / Q000139:chemically induced / Q000276:immunology*; D004195:Disease Models, Animal; D004768:Enterotoxins / Q000276:immunology; D005260:Female; D006241:Haptens / Q000009:adverse effects / Q000276:immunology*; D007073:Immunoglobulin E / Q000276:immunology; D051379:Mice; D008815:Mice, Inbred Strains; D010853:Picryl Chloride / Q000009:adverse effects / Q000276:immunology*; D013154:Spleen / Q000166:cytology / Q000276:immunology; D013211:Staphylococcus aureus / Q000276:immunology / Q000302:isolation & purification; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology
D016207:Cytokines; D004768:Enterotoxins; D006241:Haptens; D007073:Immunoglobulin E; C031818:enterotoxin B, staphylococcal; D010853:Picryl Chloride