Hepatitis B severity is associated with mitochondrial damage in T lymphocytes

Abstract Background Hepatitis B infection remains a major cause of chronic liver disease worldwide, which exerts substantial pressure on global public health security. Recent studies have demonstrated that T cell-mediated cellular immune mechanisms are important in hepatitis B progression. Oxidative stress is also an important background of numerous liver disorders, but the connections between numbers and oxidative stress of T cells remain unclear in hepatitis B. Purpose To assess the characterizations and changes of peripheral blood T lymphocytes and their mitochondrial reactive oxygen species in hepatitis B development. Methods We recruited 432 patients with hepatitis B (144 with mild disease, 165 with moderate and severe disease, 90 with compensated cirrhosis, 33 with decompensated cirrhosis) and 65 healthy people (controls) to the study. Mitochondrial damage was detected by flow cytometry with a specific probe. The immune levels of specific immune cells and T cell mitochondrial functions were evaluated with the relative and absolute counts of T lymphocyte subsets. Results Patients with hepatitis B had higher mitochondrial damage indexes, which increased with disease progression. The patients also had lower absolute CD3 + , CD4 + , and CD8 + T lymphocyte counts compared with the controls (p < 0.05), where the counts decreased with disease progression. The absolute CD8 + T cell counts were negatively correlated with the mitochondrial damage indexes (p < 0.05, r = -0.11), but there were no correlations between the absolute CD4 + T cell counts and the mitochondrial damage indexes. Furthermore, the absolute T cell counts had a weakly positive correlation with the liver injury index, but the T cell mitochondrial damage indexes were not correlated with the liver injury index. Conclusions These data suggested that the mitochondrial damage frequencies and T lymphocyte subset levels differed between the different phases of chronic HBV infection, and decreased lymphocyte subsets might be related to the increased mitochondrial damage indexes in hepatitis B patients. The abnormal change in mitochondrial function and lymphocyte subsets might be important in hepatitis B development, but the underlying mechanisms remain ambiguous.