Alarmin HMGB1 induce the activation of eosinophils by interacting with dermal fibroblasts in atopic dermatitis-like skin inflammation
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AbstractPatients with atopic dermatitis are prone to Staphylococcus aureus infection and itch-scratching-induced tissue damage, both of which are strong inducers of alarmin high mobility group box-1 protein (HMGB1) release. To better understand the in vivo role of HMGB1 in AD, the effects of anti-HMGB1 antibody on MC903-induced AD-like skin inflammation were investigated. We found that the blockage of HMGB1 pathway with anti-HMGB1 antibody alleviated the MC903-induced AD-like symptoms. The receptor for advanced glycation end products (RAGE), the HMGB1 receptor, was only detected on human eosinophils instead of human dermal fibroblasts. The stimulation of HMGB1 dose-dependently induces the release of IL-6, CXCL8 and CCL4 in eosinophil-dermal fibroblasts co-culture, as well as the increased ICAM-1 expression on dermal fibroblasts. In addition, up-regulated levels of intracellular phosphorylated nuclear factor κ light polypeptide gene enhancer in B-cell inhibitor α (pIκBα) were observed upon HMGB1 stimulation in eosinophils in co-culture with dermal fibroblasts. This study provides evidence of a pivotal role of HMGB1 in the pathogenesis of AD via the activation of eosinophils interacting with dermal fibroblasts in skin lesions.
All Author(s) ListJiao D., Wong C.K., Zhu J., Tsang M.S.M., Chu, M., Liu D.H., Chan H.Y.Z., Lam C.W.K.
Name of ConferenceAnnual Scientific Meeting of the Hong Kong Society for Immunology 2016
Start Date of Conference10/09/2016
End Date of Conference10/09/2016
Place of ConferenceHong Kong
Country/Region of ConferenceHong Kong
LanguagesEnglish-United Kingdom

Last updated on 2018-18-01 at 08:20