Crohn's and
ulcerative colitis are common conditions associated with
inflammatory bowel disease as well as intestinal flora and epithelial barrier dysfunction. A novel fermented Lactobacillus brevis (AL0035) herein assayed in a trinitro
benzene sulfonic acid (TNBS)-induced
colitis mice model after
oral administration significantly counteracted the
body weight loss and improves the disease activity index and histological injury scores. AL0035 significantly decreased the
mRNA and
protein expression of different pro-inflammatory
cytokines (TNFalpha, IL-1beta, IL-6, IL-12, IFN-gamma) and enhanced the expression of
IL-10. In addition, the probiotic promoted the expression of
tight junction proteins, such as ZO-1, keeping the intestinal mucosal barrier function to attenuate
colitis symptoms in mice. Markers of
inflammation cascade such as
myeloperoxidase (MPO) and
PPAR-gamma measured in the colon were also modified by AL0035 treatment. AL0035 was also able to reduce different lymphocyte markers' infiltration in the colon (GATA-3, T-Bet, NK1.1) and
monocyte chemoattractant protein-1 (MCP-1/CCL2), a key
chemokine involved in the migration and infiltration of monocytes/macrophages in the immunological surveillance of tissues and
inflammation. In colonic microbiota profile analysis through
16S rRNA sequencing, AL0035 increased the microbial diversity depleted by TNBS administration and the relative abundance of the Lactobacillaceae and Lachnospiraceae families, whereas it decreased the abundance of Proteobacteria. Altogether, these data indicated that AL0035 could lower the severity of
colitis induced by TNBS by regulating inflammatory
cytokines, increasing the expression of
tight junction proteins and modulating intestinal microbiota, thus preventing tissue damage induced by
colitis.