Adult ; Cytokines ; metabolism ; Female ; Hepatitis B ; complications ; Humans ; Liver Cirrhosis ; immunology ; metabolism ; pathology ; virology ; Liver Failure ; immunology ; metabolism ; pathology ; Male ; Middle Aged ; Th1 Cells ; metabolism

Antiviral Agents ; therapeutic use ; Cytokines ; metabolism ; Dendritic Cells ; immunology ; metabolism ; pathology ; Endotoxemia ; complications ; pathology ; Hepatitis B ; complications ; pathology ; Humans ; Hypoxia ; complications ; pathology ; Ischemia ; complications ; pathology ; Liver ; metabolism ; pathology ; Liver Failure ; etiology ; immunology ; pathology ; therapy ; T-Lymphocytes ; immunology ; pathology

Bacterial Translocation ; physiology ; Humans ; Intestinal Mucosa ; pathology ; physiology ; Lipopolysaccharides ; metabolism ; physiology ; Liver Failure, Acute ; etiology ; immunology ; physiopathology ; Lymphocytes ; immunology ; metabolism ; Macrophages ; immunology ; metabolism ; Signal Transduction ; genetics ; physiology ; Toll-Like Receptor 4 ; metabolism ; physiology

PURPOSE: Acute hepatitis A (AHA) and acute hepatitis B (AHB) are caused by an acute infection of the hepatitis A virus and the hepatitis B virus, respectively. In both AHA and AHB, liver injury is known to be mediated by immune cells and cytokines. In this study, we measured serum levels of various cytokines and T-cell cytotoxic proteins in patients with AHA or AHB to identify liver injury-associated cytokines. MATERIALS AND METHODS: Forty-six patients with AHA, 16 patients with AHB, and 14 healthy adults were enrolled in the study. Serum levels of 17 cytokines and T-cell cytotoxic proteins were measured by enzyme-linked immunosorbent assays or cytometric bead arrays and analyzed for correlation with serum alanine aminotransferase (ALT) levels. RESULTS: Interleukin (IL)-18, IL-8, CXCL9, and CXCL10 were significantly elevated in both AHA and AHB. IL-6, IL-22, granzyme B, and soluble Fas ligand (sFasL) were elevated in AHA but not in AHB. In both AHA and AHB, the serum level of CXCL10 significantly correlated with the peak ALT level. Additionally, the serum level of granzyme B in AHA and the serum level of sFasL in AHB correlated with the peak ALT level. CONCLUSION: We identified cytokines and T-cell cytotoxic proteins associated with liver injury in AHA and AHB. These findings deepen the existing understanding of immunological mechanisms responsible for liver injury in acute viral hepatitis.
Acute Disease ; Adult ; Alanine Transaminase/blood ; Biomarkers/blood ; Cytokines/*blood ; Enzyme-Linked Immunosorbent Assay ; Fas Ligand Protein/blood ; Female ; Hepatitis A/blood/virology ; Hepatitis A virus/*genetics/immunology ; Hepatitis B/blood/virology ; Hepatitis B virus/*genetics/immunology ; Humans ; Interleukin-6/blood ; Interleukin-8/blood ; Interleukins/blood ; Liver Failure/immunology/metabolism/*pathology ; Male ; Middle Aged ; T-Lymphocytes, Cytotoxic/immunology/*metabolism