Under the pathological conditions of aggravated bacterial infection and UC, the tight junctions of intestinal epithelial cells are disrupted, cell permeability increases, and the intestinal barrier is destroyed, causing massive infiltration of immune cells and upregulation of inflammatory cytokine (i.e., TNF-α, IL-1, and FOS) expression, which promotes apoptosis of intestinal epithelial cells and increases permeability, further destroying the intestinal barrier and further aggravating local intestinal mucosal damage [30–33]. This evidence concerns the gene FOS and bacterial infectious disease.