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

• Published in: Journal of translational medicine 2015-09, Vol.13 (1), p.310, Article 310
• Main Authors: Jhun, JooYeon, Lee, SeungHoon, Kim, HeeYeon, Her, Yang-Mi, Byun, Jae Kyeong, Kim, Eun-Kyung, Lee, Soon Kyu, Cho, Mi-La, Choi, Jong Young
• Format: Article
• Language: English
• Subjects: Adult; Care and treatment; Case-Control Studies; Chromosomal proteins; Communicable diseases; Complications and side effects; Computer software industry; Enzyme-Linked Immunosorbent Assay; Enzymes; Female; Gene Expression Regulation; Hepatitis B; Hepatitis B - blood; HMGB1 Protein - metabolism; Humans; Immunohistochemistry; Inflammation; Interleukin-17 - metabolism; Interleukin-1beta - metabolism; Interleukins; Liver - metabolism; Male; Microscopy, Confocal; Microscopy, Fluorescence; Middle Aged; p38 Mitogen-Activated Protein Kinases - metabolism; Prospective Studies; Real-Time Polymerase Chain Reaction; Receptor for Advanced Glycation End Products - metabolism; Receptors, Immunologic - metabolism; Risk factors; RNA; RNA, Messenger - metabolism
• ISSN: 1479-5876; 1479-5876
• DOI: 10.1186/s12967-015-0663-1

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. Mild and severe HB liver tissue and peripheral blood samples were obtained intra-operatively. Histological analysis of the livers was performed by immunohistochemistry. IL-1β 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. 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-1β 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-1β in peripheral blood cells HB patients with ACLF. 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.