Bitter side of sweet: A stage-dependent immunometabolic model linking metabolic syndrome and inflammatory bowel disease

Figure 2 Proposed immunological features associated with advanced metabolic dysfunction in ulcerative colitis. The figure summarizes immunological observations identified in ulcerative colitis patients with metabolic characteristics consistent with advanced or late-stage of metabolic syndrome. Impaired intestinal barrier integrity may be associated with increased activation of dendritic cells and M1-polarized macrophages, accompanied by enhanced T helper cell (Th) 1- and Th17-associated immune responses. These immune populations are linked to increased production of interferon-γ, interleukin-17, and other pro-inflammatory mediators, together with greater recruitment of innate immune cells. Concurrently, reduced regulatory immune activity and predominance of pro-inflammatory signaling pathways have been observed in association with increased inflammatory burden and epithelial injury. CVD: Cardiovascular disease; NAFLD: Non-alcoholic fatty liver disease; IL: Interleukin; TLR: Toll-like receptor; Th1: T helper type 1 cells; Th0: T helper type 0 cells; Th17: T helper type 17 cells; IFN: Interferon; TNF: Tumor necrosis factor.