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Lipoteichoic acid from Staphylococcus aureus induces Th2-prone dermatitis in mice sensitized percutaneously with an allergen

Authors


Correspondence:Katsuhiko Matsui, Department of Immunobiology, Meiji Pharmaceutical University, 2–522–1 Noshio, Kiyose, Japan. E-mail: kmatsui@my-pharm.ac.jp

Summary

Background We found previously that lipoteichoic acid (LTA) from Staphylococcus aureus has the ability to induce Th2 cytokine production by peripheral blood mononuclear cells (PBMC) from patients with atopic dermatitis (AD). However, it is not known whether LTA can induce a Th2-dominant cytokine response in the skin of AD patients.

Objective The purpose of this study was to determine the effects of LTA in mice sensitized percutaneously with a house dust mite antigen (MA) through barrier-disrupted skin, as an experimental animal model of AD.

Methods Mice were sensitized with MA by a single topical application to barrier-disrupted abdominal skin. Seven days after the sensitization, the mice were challenged on the dorsal skin by LTA to elicit localized skin inflammation. The cytokine response in the dorsal skin was investigated by reverse transcription-polymerase chain reaction (RT-PCR) and immunohistological analysis. The infiltration of inflammatory cells in the skin was also observed by histological staining.

Results Injection of LTA into the dorsal skin of MA-sensitized mice, which show a Th2-dominant cytokine response against the homologous antigen, increased the expression of mRNA for IFN-γ, IL-4 and IL-5, but not IL-2. Immunohistological analysis demonstrated that levels of IFN-γ, IL-4 and IL-5 transcripts corresponded with those of protein synthesis. In addition, the dorsal skin of MA-sensitized mice challenged with LTA showed significantly increased numbers of neutrophils, eosinophils, mononuclear cells and mast cells compared with control mice challenged with LTA.

Conclusion These results suggest that LTA has the ability to induce localized Th2-prone dermatitis in an allergen-independent manner in the skin of AD patients and may explain the role of colonization with S. aureus in AD patients.

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