Anti-inflammatory potential of Lactobacillus plantarum LS/07 in acute colitis in rats

Abstract

To evaluate the effi ciency of the probiotic strain Lactobacillus plantarum LS/07 in dextran sulphate sodium (DSS) induced acute colitis selected biochemical (activity of β-glucuronidase), microbiological (counts of lactobacilli and coliforms), and immunological (IL-6, IL-8, IL-13, NF-κB, MPO) parameters were assessed. SpragueDawley rats were divided into groups: Control, Acute colitis, and Probiotic. Acute colitis was induced using 5% DSS in drinking water for 7d. DSS induced an infl ammatory process in the colonic tissue, increased the activity of β-glucuronidase (p<0.001), increased the counts of coliform bacteria and decreased lactobacilli counts (p<0.05), and activated the production of the measured parameters (NF-κB, MPO, IL-6, IL-8) except of IL-13. Lactobacillus plantarum LS/07 in the diet alleviated the DSS induced infl ammatory process by inhibiting the production of IL-6, IL-8, the activities of NF-κB and MPO, and stimulated the production of IL-13. The probiotic reduced the activity of β-glucuronidase (p<0.05), increased lactobacilli counts and decreased coliform bacteria. These results indicate that di etary intake of Lactobacillus plantarum LS/07 suppressed the expression of markers playing an important role in the infl ammatory process. We conclude that the anti-infl ammatory properties of Lactobacillus plantarum LS/07 makes its suitable for the prevention or treatment of colitis.

Probiotic Effector Compounds: Current Knowledge and Future Perspectives

“…This was demonstrated when E. coli Nissle 1917 colonized pigs showed a higher gut IgA response relative to L. rhamnosus GG colonization ( Kandasamy et al, 2016 ). The anti-inflammatory ability of L. plantarum in acute colitis mice ( Emília et al, 2018 ) has at least in part been attributed to the presence of a small domain of the surface layer protein of the bacterium. These surface layer proteins have been shown to bind to a mannose receptor in gut epithelial cells to prevent p38 MAPK phosphorylation by inhibiting the Toll-like receptor (TLR) 5 pathway ( Liu et al, 2012 ) during inflammatory conditions.…”