Lactobacillus johnsonii colonizing in mice intestine contributes to control the gut barrier function via regeneration of the crypt in DSS-treated mice

Abstract

Background

Unbalanced gut microbiota is considered to cause dysfunction of the gut barrier function. Lactobacillus johnsonii MG, isolated from mouse feces as gut associating lactobacilli, enhanced gut barrier function in Caco-2 cells via interaction with JAM-2 in tight junctions. In this study, the anti-inflammatory effects of L. johnsonii MG were investigated in a colitis mouse model developed by treating mice with 3% dextran sulfate sodium (DSS) for 9 days.

Results

MG treatment of colitis mice resulted in fast recovery of the body weight and showed significant improvement in the disease activity index and histopathological scores. The histomorphological score increased by DSS treatment was significantly improved in the MG-treated group. In the intestine, the expression of Ocln, Zo1, Itga6, Lama3, and Jam2 genes, which are involved in tight junction functions, were significantly upregulated in MG-treated colitis mice. In the microflora analysis, the abundance of Ruminococcaceae, Bacteroides, and Lachnospiraceae were reduced in DSS-treated mice and recovered by MG treatment.

Conclusion

We reported the potential of L. johnsonii MG in the regeneration of crypts and integrity of matrix proteins in the gut of mice with colitis through its association with tight junctions. The experimental results provide new insights into the probiotic effect of tight junction associating L. johnsonii MG.