The synergic impact of lignin and Lactobacillus plantarum on DSS-induced colitis model via regulating CD44 and miR 199a alliance

World J Microbiol Biotechnol. 2022 Oct 12;38(12):233. doi: 10.1007/s11274-022-03424-z.

Abstract

Chronic or recurrent immune system activation and inflammation inside the gastrointestinal tract is characterized by inflammatory bowel disease (IBD). Due to the lack of safety and efficacy of traditional medications, the use of food supplements for IBD management is on the rise. Numerous studies reported that, certain food supplements have a variety of therapeutic benefits for IBD. In the present study, a mouse model of IBD was used to the anti-colitis effects of lignin supplementation with Lactobacillus plantarum (L. plantarum) on intestinal inflammation. The animal model was treated with dextran sodium sulphate (DSS), the illness index increased, and colon length and body weight declined, but these effects were reversed when lignin and L. plantarum treated groups. In addition, lignin and L. plantarum supplementation inhibited the DSS induced increase in levels of cytokines TNF-α (250 pg/mL), INF-γ (180 pg/mL), IL-1β (70 pg/mL) and TGF- β (72 pg/mL). Gene and protein expression study revealed that Lignin and L. plantarum supplementation restored the expression of E-cad and suppressed the expression of STAT3 in DSS induced colitis model. Lignin and L. plantarum supplementation also suppressed CD44 expression (1.2 fold) by up regulating the expression of miR199a (1 fold) over DSS induced colitis. Our study suggests that Lactobacillus, lignin, and their synergistic treatments have protective roles against inflammatory bowel disease through changes in inflammatory cytokines, and miR 199a expression in DSS-induced colitis.

Keywords: DSS; Inflammatory bowel disease; L. plantarum; Lignin; miR199a.

MeSH terms

  • Animals
  • Colitis* / chemically induced
  • Colitis* / drug therapy
  • Colon / metabolism
  • Cytokines / metabolism
  • Dextran Sulfate / adverse effects
  • Disease Models, Animal
  • Hyaluronan Receptors* / genetics
  • Hyaluronan Receptors* / metabolism
  • Inflammation / drug therapy
  • Inflammatory Bowel Diseases* / chemically induced
  • Inflammatory Bowel Diseases* / drug therapy
  • Lactobacillus plantarum* / metabolism
  • Lignin / metabolism
  • Mice
  • Mice, Inbred C57BL
  • MicroRNAs* / metabolism
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Cd44 protein, mouse
  • Cytokines
  • Hyaluronan Receptors
  • MicroRNAs
  • Mirn199 microRNA, mouse
  • Tumor Necrosis Factor-alpha
  • Lignin
  • Dextran Sulfate