When metabolic disease rewrites infection biology: Long-term multiorgan consequences of Helicobacter pylori infection in diabetes

Figure 1 Proposed mechanistic pathway from Helicobacter pylori infection under diabetic conditions to multiorgan injury. The stepwise pathway depicts: (1) Impaired mucosal immunity allowing prolonged gastric colonization; (2) Irreversible mucosal fibrosis and inflammation; (3) Exosome/outer membrane vesicles-mediated extra-gastric antigen translocation via the portal circulation; (4) Hepatic NF-κB activation and non-alcoholic fatty liver disease progression; (5) Renal cytokine-mediated podocyte injury; (6) Compounded microbiota dysbiosis with metabolic endotoxemia; and (7) Convergent systemic apoptotic signalling. NAFLD: Non-alcoholic fatty liver disease; OMV: Outer membrane vesicles; NASH: Non-alcoholic steatohepatitis; IL: Interleukin; TNF-α: Tumor necrosis factor-alpha; SCFA: Short-chain fatty acid; LPS: Lipopolysaccharide; H. pylori: Helicobacter pylori.