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Increased serum HMGB 1 levels in patients with H enoch– S chönlein purpura
Author(s) -
Chen Tao,
Guo Zaipei,
Wang Wenju,
Qin Sha,
Cao Na,
Li Mengmeng
Publication year - 2014
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/exd.12422
Subject(s) - cytokine , western blot , immunology , henoch schonlein purpura , medicine , antibody , microbiology and biotechnology , chemistry , biology , vasculitis , pathology , biochemistry , disease , gene
High‐mobility group box‐1 ( HMGB 1) has been implicated as a pro‐inflammatory cytokine in the pathogenesis of various inflammatory and autoimmune diseases. However, information about HMGB 1 in H enoch– S chönlein purpura ( HSP ) is still unclear. Herein, we investigated the role of HMGB 1 in patients with HSP and the pro‐inflammatory effects of HMGB 1 on human dermal microvascular endothelial cell line ( HMEC ‐1). Serum HMGB 1 levels in patients with HSP together with patients with allergic vasculitis ( AV ) and urticarial vasculitis ( UV ) were detected by enzyme‐linked immunosorbent assay ( ELISA ). HMEC ‐1 cells were treated with HMGB 1 at concentrations ranging from 4 ng/ml to 100 ng/ml. Serum HMGB 1 levels were significantly increased in patients with HSP , AV and UV , when compared with those in control group. Moreover, abundant cytoplasmic expression of HMGB 1 was observed in endothelial cells in lesional skin of HSP patients. Using membrane cytokine antibody array, we indicate that HMGB 1 markedly induced TNF ‐ α and IL ‐6 release in cultured supernatant. Furthermore, by real‐time quantitative PCR and ELISA , the effects of HMGB 1 on these cytokines production in HMEC ‐1 cells were established. Finally, Western blot data revealed that HMGB 1 can induce phosphorylation of inhibitor of κ B ‐ α ( I κ B α ) and the nuclear translocation of nuclear factor‐ κ B ( NF ‐ κ B ) p65 in HMEC ‐1 cells. In conclusion, this study provides first observations on the association of HMGB 1 with HSP . We suggest that HMGB 1 may be an important mediator of endothelial inflammation through the induction of TNF ‐ α and IL ‐6 production and may play a crucial role in the pathogenesis of HSP .