H89 Treatment Reduces Intestinal Inflammation and Overgrowth in Mice.
Fiche publication
Date publication
décembre 2020
Journal
Microorganisms
Auteurs
Membres identifiés du Cancéropôle Est :
Pr BETTAIEB Ali
Tous les auteurs :
Dumortier C, Charlet R, Bettaieb A, Jawhara S
Lien Pubmed
Résumé
Deregulation of the dynamic crosstalk between the gut microbiota, intestinal epithelial cells, and immune cells is critically involved in the development of inflammatory bowel disease and the overgrowth of opportunistic pathogens, including the human opportunistic fungus . In the present study, we assessed the effect of N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide (H89), a protein kinase A inhibitor, on the migration of macrophages to through dextran sulphate sodium (DSS)-challenged Caco-2 cells. We also investigated the impact of H89 on intestinal inflammation and clearance from the gut, and determined the diversity of the gut microbiota in a murine model of DSS-induced colitis. H89 reduced the migration of macrophages to through DSS-challenged Caco-2 cells. In addition, H89 decreased viability and diminished the expression of pro-inflammatory cytokines and innate immune receptors in macrophages and colonic epithelial Caco-2 cells. In mice with DSS-induced colitis, H89 attenuated the clinical and histological scores of inflammation and promoted the elimination of from the gut. H89 administration to mice decreased the overgrowth of and populations while populations increased significantly. Overall, H89 reduced intestinal inflammation and promoted the elimination of from the gut.
Mots clés
Candida albicans, DSS, Enterococcus faecalis, Escherichia coli, H89, Lactobacillus johnsonii, colitis, microbiota, protein kinase A
Référence
Microorganisms. 2020 Dec 19;8(12):