Intestinal immune barrier integrity in rats with nonalcoholic hepatic steatosis and steatohepatitis

Nonalcoholic fatty liver disease (NAFLD) has emerged as the major cause of chronic liver injury. Intestinal barrier plays an important role in the pathogenis of NAFLD. The aim of this article was to assess intestinal immune barrier function during the development of NAFLD.

Totally 60 male Sprague-Dawley (SD) rats were divided into 2 groups: normal diet (ND) group and high-fat diet (HFD) group. NAFLD rat model was established in the HFD rat group. Portal blood endotoxin level was assessed by limulus test. The percentage of CD4+ cells and CD8+ cells in peripheral blood mononuclear cells (PBMC) and lymphocytes in Peyer's patches (PP) were analysed by flow cytometry. Intestinal secretory immunoglobulin A (SIgA) level was evaluated by enzyme-linked immunosorbent assay. Paired Student's t test was used for the statistic analysis.

HFD rats presented with simple steatosis at the 4th and 8th week and progressed to nonalcoholic steatohepatitis at the 12th week. Elevated lipopolysaccharides (LPS) level in HFD rats was observed at the 8th week ((1.54 ± 0.30) times of ND group, P < 0.01). CD4/CD8 ratios in PBMC and PP of HFD rats were increased at the 4th week ((1.50 ± 0.47) and (1.63 ± 0.34) times of ND group, P < 0.05) and decreased at the 8th week ((0.50 ± 0.16) and (0.61 ± 0.26) times of ND group, P < 0.05). At the 12th week, CD4/CD8 ratio ((1.47 ± 0.46) times, P < 0.05) in PP increased to levels observed in the 4th week. Intestinal SIgA expression of HFD rats was remarkably up-regulated at 12th week ((2.70 ± 1.65) times, P < 0.05).

Liver-gut axis in rats with NAFLD may mediate and improve intestinal immune function by increased CD4/CD8 ratio in PP and increased production of SIgA.