APASL 2017 - The 26th Conference of the Asian Pacific Association for the Study of the Liver will be held in Shanghai, China on February 15-19, 2017.
APASL 2017 - The 26th Conference of the Asian Pacific Association for the Study of the Liver covers topics such as: new developments, research updates and technological advancements in the study of Liver, including:
Autoimmune hepatitis and cholestatic liver disease
Drug Induced Liver Disease (DILD)
Other viral hepatitis
Portal hypertension and cirrhosis - Pathophysiology and Clinical
Cholangioca and other liver neoplasm
Cholelithiasis and biliary tract disease
Case report and case series
APASL 2017 - The 26th Conference of the Asian Pacific Association for the Study of the Liver brings together physicians, clinicians, researchers, scientists, nurses, academics, residents and allied health professionals in hepatology and related fields including pathology, gastroenterology, surgery, radiology, oncology, virology, and others.
BACKGROUND: Hepatitis B virus (HBV) 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/NF-kB aggravates inflammation enhancing the expression of interleukin (IL)-23.
METHODS: Baseline serum HMGB1, IL-6, IL-12, IL-17, IL-23, TNF-α, and IFN-γ was analyzed using from inactive HBsAg carrier state (IC), chronic hepatitis B (CHB), HBV-related acute-on-chronic liver failure (HBV-ACLF) patients and healthy individuals who served as healthy controls (HCs). Purified monocytes were isolated from peripheral blood and induced into monocyte-derived dendritic cells (MoDCs), HMGB1, NF-κB, IL-23 and IL-23R expression in MoDCs from 4 groups was analyzed using real-time PCR and flow cytometric analysis. HMGB1, HBsAg, HBeAg and HBcAg in vitro stimulate MoDCs. The siRNA against NF-κB and overexpression of NF-κB was utilized to assess the impact of NF-κB on pro-inflammatory properties.
RESULTS: Baseline serum HMGB1 and IL-23 were significantly upregulated in non-survival compared with survival of HBV-ACLF patients. Serum HMGB1 and IL-23 downregulated in survival after treatment, whereas even upregulated in non-survival of HBV-ACLF patients. HMGB1, HBsAg, HBeAg and HBcAg in vitro stimulation induced the expression of NF-Kb and IL-23 in MoDCs of HCs. On the other hands, nuclear factor-kappa B regulated the expression of IL-23 in monocyte-derived dendritic cells of HBV-ACLF patients.
CONCLUSIONS: High baseline serum HMGB1 and IL-23 are associated with HBV-ACLF patient mortality. HMGB1/NF-KB contribute to the inflammation enhancing the expression of IL-23 by MoDCs, which mediates damage-induced liver inflammation in HBV-ACLF patients .