has indicated that IL-10 reduces colonic inflammation in mice with colitis by inhibiting lipopolysaccharide-induced glucose uptake and glycolysis in macrophages while promoting OXPHOS; furthermore, in macrophages from colitis mice and patients with IBD, a deficiency of IL-10 exacerbates mitochondrial damage and enhances the activation of mTORC1 signaling, leading to increased expression of NLRP3 and IL-1β (85). This evidence concerns the gene IL10 and inflammatory bowel disease.