High mobility group box 1 is increased in the sera of psoriatic patients with disease progression

Background Psoriasis vulgaris (PV) is an autoimmune‐related chronic inflammatory disease, which appears mostly in skin, but also affects the vascular and metabolic system. The incidence of PV is 2–3% in the general population and there is still no possibility to cure. Trigger factors have been ident...

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Published in:Journal of the European Academy of Dermatology and Venereology 2016-03, Vol.30 (3), p.435-441
Main Authors: Bergmann, C., Strohbuecker, L., Lotfi, R., Sucker, A., Joosten, I., Koenen, H., Körber, A.
Format: Article
Language:English
Subjects:
Adult
Apoptosis
Disease Progression
Enzyme-Linked Immunosorbent Assay
Female
HMGB1 Protein - metabolism
Humans
Male
Middle Aged
Psoriasis - diagnosis
Psoriasis - metabolism
Skin - metabolism
Skin - pathology
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Summary:Background Psoriasis vulgaris (PV) is an autoimmune‐related chronic inflammatory disease, which appears mostly in skin, but also affects the vascular and metabolic system. The incidence of PV is 2–3% in the general population and there is still no possibility to cure. Trigger factors have been identified to initiate and maintain inflammation in the skin, which is characterized by Th1‐, Th17‐ and Th22‐ cells. Objective We hypothesize that the damage‐associated molecular pattern (DAMP) molecule high mobility group box 1 (HMGB1) plays a role in the pathogenesis of PV. HMGB1 is a DNA‐binding protein located in the nucleus, which acquires cytokine‐like properties once released from the cell upon necrotic cell death or actively secreted by immune cells in inflammation and cancer. Methods We recruited 90 psoriatic patients under and without therapy with mild, intermediate and severe progression of disease, defined by the Psoriasis Area Severity Index. Serum levels of HMGB1 in patients with PV were detected by enzyme‐linked immunosorbent assay (ELISA). Results Our results show an increased level of HMGB1 in the sera of patients with PV in comparison to healthy donors. Furthermore, our analyses reveal that HMGB1 levels are significantly increased with disease progression and are downregulated after standard therapies for PV have been conducted. Conclusion Our data provide insights into a possible role of HMGB1 for inflammation in PV.
ISSN:0926-9959
1468-3083
DOI:10.1111/jdv.13564