HMGB1/RAGE induces IL-17 expression to exaggerate inflammation in peripheral blood cells of hepatitis B patients

作者：Jhun JooYeon; Lee SeungHoon; Kim HeeYeon; Her Yang Mi; Byun Jae Kyeong; Kim Eun Kyung; Lee Soon Kyu; Cho Mi La^*; Choi Jong Young

来源：Journal of Translational Medicine, 2015, 13(1): 310.

DOI：10.1186/s12967-015-0663-1

• HMGB1
• RAGE
• IL-17
• Inflammation
• Hepatitis B virus

Background: Hepatitis B (HB) is an infectious disease with unfavorable consequence for patients and involved in chronic inflammation of liver. The present study aimed to investigate whether High-mobility group protein B (HMGB) 1/receptor for advanced glycation end products (RAGE) aggravates inflammation enhancing the expression of interleukin (IL)-17.
Methods: Mild and severe HB liver tissue and peripheral blood samples were obtained intra-operatively. Histological analysis of the livers was performed by immunohistochemistry. IL-1 beta and IL-6 of liver tissue were detected by confocal microscopy staining. Relative mRNA expression was measured by real-time PCR and protein levels were measured by enzyme-linked immunosorbent assay.
Results: HMGB1, RAGE and IL-17 expression is increased in liver of HB patients with acute on chronic liver failure (ACLF) compared to healthy controls. HMGB1 treatment induced inflammatory cytokines including IL-17 in peripheral blood cells of HB patients. IL-17 also induced the expression of RAGE and IL-1 beta in peripheral blood cells of HB patients with ACLF. On the other hands, the inhibitory factor of p38 and nuclear factor-kappa B reduced the expression of RAGE and IL-1 beta in peripheral blood cells HB patients with ACLF.
Conclusions: HMGB1, RAGE and IL-17 expression is increased in liver of severe HB patients. HMGB1 and RAGE interaction may contribute to the inflammation of liver enhancing the expression of IL-17, which can be possibly restored through the decline of the HMGB1/RAGE axis.

• 出版日期2015-9-21
• 单位河北医科大学