Lactobacillus plantarum AN1 cells increase caecal L. reuteri in an ICR mouse model of dextran sodium sulphate-induced inflammatory bowel disease.

To clarify the different effects of live and heat-killed probiotics on inflammatory bowel disease (IBD), the anti-inflammatory and protective effects of Lactobacillus plantarum AN1 cells isolated from the fermented fish aji-narezushi on murine macrophage RAW264.7 cells and in ICR mice with dextran sodium sulphate (DSS)-induced IBD were determined. L. plantarum AN1 cells showed anti-inflammatory activities in vitro, indicated by secretion of nitric oxide (NO) from RAW264.7 cells in the presence and absence of Escherichia coli 0111 lipopolysaccharide (LPS). L. plantarum AN1 cells also protected RAW264.7 cells against hydrogen peroxide toxicity. There was no difference between these effects in heat-killed and ultraviolet irradiation-killed cells. In the murine IBD model, both live and heat-killed L. plantarum AN1 cells via drinking water tended to ameliorate atrophy of colon length, mucosal tissue damage, and spleen enlargement. Amplicon sequencing of 16S rDNA (V4) revealed that both live and heat-killed AN1 cells increased abundance of indigenous lactic acid bacteria, particularly Lactobacillus reuteri. The results suggest that increased indigenous lactic acid bacterial abundance and feeding with L. plantarum AN1 cells synergistically improve effects against IBD.