MORPHOLOGICAL STUDY OF COLONIC MUCOSA IN MICE WITH DEXTRAN SULFATE SODIUM-INDUCED COLITIS: THE IMPACT OF PROBIOTIC SUPPLEMENTATION

Inflammatory bowel diseases (IBD) are chronic gastrointestinal disorders that can impair the patient’s quality of life.1 Dextran sulfate sodium (DSS)-induced colitis is one of the most common mice models of chemically induced IBD.2 The treatments for IBD showed insufficient therapeutic efficacy. Many studies identified dietary supplementation with probiotics as a promising intervention by alleviating clinical symptoms. The potential properties of Weissella paramesenteroides A1 (Wp) and Pediococcus acidilactici 46A (Pa) were evaluated on a murine model of DSS-induced colitis. 8-week-old mice were used. Colitis was induced by administering 3% (w/v) DSS in drinking water for 7 days. Probiotics were supplemented orally (1 × 108 CFU daily) for 10 days before DSS administration. Weight loss, stool consistency and intestinal bleeding were monitored to evaluate the clinical progression of colitis. Microscopically, histological damage, inflammatory cells infiltration and pro-inflammatory cytokines expression were assessed on proximal and distal colon sections. Pa supplementation was able to reduce the macroscopic severity score while not affecting weight loss. The histological damage was recorded for impairment of crypts architecture, goblet cells depletion and inflammatory infiltrate. The colitis severity was reduced in the Pa pretreated mice compared to the DSS group. The presence of CD3+ cells was lower in the Pa pretreated animals compared to DSS. The same pattern was observed in the sections incubated with TNF-α antibodies. Particularly in the Pa treated mice was appreciated a reduction of inflammatory cells in the area in which the colonic wall cytoarchitecture was maintained. These results showed the potential use of specific strains of bacteria to treat intestinal disorders. Pa is active against intestinal inflammation in DSS-induced colitis although further studies are necessary to better characterize its possible implication as a therapeutic agent against IBD. References 1. Mentella MC et al. Nutrients 2020;29;12:944. 2. Chassaing B et al. Curr Protoc Immunol 2014;104:15.25.1-14.