MORPHOLOGICAL MODULATION OF COLONIC ENTERIC PLEXI IN MICE MODEL OF COLITIS AND THE POSSIBLE EFFECTS OF BACTERIAL STRAIN SUPPLEMENTATION

Inflammatory bowel diseases (IBD) are gastrointestinal disorders associated with altered intestinal permeability, which causes a degeneration of the enteric plexi of the enteric nervous system (ENS). Treatments for IBD show poor efficacy. Many studies have identified probiotic supplementation as a possible method for alleviating clinical symptoms. The potential properties of Pediocuccus acidilactici 46A (Pa) were evaluated on a murine model of Dextran sulfate sodium (DSS)-induced colitis as models of chemically induced IBD. Colitis was induced in 8-week-old mice, administering 2.5% (w/v) DSS in drinking water for 7 days. Pa was supplemented orally (1×108 CFU daily) for 10 days before DSS administration. General conditions, body weight loss, stool characteristics, and occult blood were monitored to evaluate the clinical progression of colitis. Histological damage, neurodegeneration, and pro-inflammatory cytokines expression were detected on proximal and distal colon sections and the histological index scoring was evaluated. Pa in the pretreated mice was able to reduce the colitis severity while not affecting weight loss, compared to the DSS group. Defects of enteric glial cells (EGCs) function and localization, barrier integrity dysfunction, and immune cell infiltrations were observed in colitis-induced groups and a positive improvement was evidenced in Pa-supplemented groups. Morphological modification of neurons of the myenteric plexus was assessed by evaluating HuC/D pan-neuronal marker, then colonic nitrergic and cholinergic pathways were focused, and a neurodegeneration was appreciated in DSS-mice. These results demonstrate that Pa seems to counteract colonic mucosal degeneration and neuronal alteration. However, further studies are needed to demonstrate the use of specific bacterial strains to manage intestinal disorders and correlated ENS modulation in IBD.