NFKB1 and colitis: The failure to maintain an intact intestinal epithelium and to repair DSS-induced intestinal epithelial damage would result in an increased uptake of luminal antigens, including bacteria and bacterial products, and thus lead to the activation of underlying immune cells and the mounting of an inflammatory response: In the DSS model of acute chemical-induced colitis, luteolin's foremost impact is likely geared towards enterocytes, inhibiting NF-κB-dependent protective molecules.