Expression of Human Glucocorticoid Receptor in T Lymphocytes in Acute-on-Chronic Hepatitis B Liver Failure

Background Glucocorticoid receptor (GR) participates in the pathogenesis of liver inflammation. However, the potential role of GR in acute-on-chronic hepatitis B liver failure (ACHBLF) is still obscure. Aim This present study was aimed to determine peripheral GR expression in ACHBLF patients. Methods Forty patients with ACHBLF, 20 patients with chronic hepatitis B (CHB) and 16 healthy controls were included in this retrospectively study. Flow cytometry was used to determine the peripheral expression of GR ? T lymphocytes. Semi-quantitative reverse transcription polymerase chain reaction (RT–PCR) was performed for assessing relative mRNA levels of GR alpha and beta isoforms in peripheral blood mononuclear cells. Serum cortisol level was evaluated using radioimmunoassay. Results The serum cortisol level and the percentage of GR ? T lymphocytes inACHBLF patients were significantly decreased compared with CHB patients and healthy controls. However, there were no significant differences in mean fluorescence intensity (MFI) of GR ? T lymphocytes within three groups. The relative GR alpha mRNA expression in ACHBLF patients was significant decreased compared with healthy controls. However, the relative GR beta mRNA expression in ACHBLF patients was significantly increased compared with CHB patients and healthy controls. In ACHBLF patients, the percentage of GR ? T lymphocyte was significantly positively associated with relative GR alpha expression, prothrombin activity, and HBV DNA level, but negatively correlated with serum cortisol level and MELD score. Furthermore, the percentage of GR ? T lymphocytes was also obviously elevated in survivors than non-survivors. Conclusions It was strongly suggested that GR play an important role in the pathogenesis of ACHBLF.