Lactobacillus pentosus strain S-PT84 improves steatohepatitis by maintaining gut permeability

in Journal of Endocrinology
View More View Less
  • 1 Y Sakai, Advanced Preventive Medical Sciences Research Center, Kanazawa University, Kanazawa, Japan
  • 2 H Arie, Division of Health Sciences, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Japan
  • 3 Y Ni, Advanced Preventive Medical Sciences Research Center, Kanazawa University, Kanazawa, Japan
  • 4 F Zhuge, Advanced Preventive Medical Sciences Research Center, Kanazawa University, Kanazawa, Japan
  • 5 L Xu, Advanced Preventive Medical Sciences Research Center, Kanazawa University, Kanazawa, Japan
  • 6 G Chen, Advanced Preventive Medical Sciences Research Center, Kanazawa University, Kanazawa, Japan
  • 7 N Nagata, Advanced Preventive Medical Sciences Research Center, Kanazawa University, Kanazawa, Japan
  • 8 T Suzuki, Department of Biofunctional Science and Technology, Hiroshima University, Higashihiroshima, Japan
  • 9 S Kaneko, Advanced Preventive Medical Sciences Research Center, Kanazawa University, Kanazawa, Japan
  • 10 T Ota, Advanced Preventive Medical Sciences Research Center, Kanazawa University, Kanazawa, Japan
  • 11 M Nagashimada, Advanced Preventive Medical Sciences Research Center, Kanazawa University, Kanazawa, Japan

Correspondence: Mayumi Nagashimada, Email: nakanaga@staff.kanazawa-u.ac.jp
Restricted access

Intestinal mucosal barrier dysfunction is closely related to the pathogenesis of nonalcoholic steatohepatitis (NASH). Gut immunity has been recently demonstrated to regulate gut barrier function. The Lactobacillus pentosus strain S-PT84 activates helper T cells and natural killer/natural killer T cells. In this study, we examined the effect of S-PT84 on NASH progression induced by high-cholesterol/high-fat diet (CL), focusing on the immune responses involved in gut barrier function. C57BL/6 mice were fed a normal chow or CL diet with or without 1 × 1010 S-PT84 for 22 weeks. S-PT84 administration improved hepatic steatosis by decreasing triglyceride and free fatty acid levels by 34% and 37%, respectively. Furthermore, S-PT84 inhibited the development of hepatic inflammation and fibrosis, suppressed F4/80+ macrophage/Kupffer cell infiltration, and reduced liver hydroxyproline content. Administration of S-PT84 alleviated hyperinsulinemia and enhanced hepatic insulin signalling. Compared with mice fed CL diet, mice fed CL+S-PT84 had 71% more CD11c-CD206+ M2 macrophages, resulting in a significantly decreased M1/M2 macrophage ratio in the liver. Moreover, S-PT84 inhibited the CL diet-mediated increase in intestinal permeability. Additionally, S-PT84 reduced the recruitment of interleukin-17-producing T cells and increased the levels of intestinal tight junction proteins, including zonula occludens-1, occludin, claudin-3, and claudin-7. In conclusion, our findings suggest that S-PT84 attenuates diet-induced insulin resistance and subsequent NASH development by maintaining gut permeability. Thus, S-PT84 represents a feasible approach to prevent the development of NASH.

 

      Society for Endocrinology

Sept 2018 onwards Past Year Past 30 Days
Abstract Views 97 97 97
Full Text Views 14 14 14
PDF Downloads 2 2 2