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

Figure 2 Schematic overview of the host-pathogen-metabolic axis in diabetic Helicobacter pylori infection. Hyperglycaemia-driven immune suppression prolongs H Helicobacter pylori gastric colonization, triggering progressive mucosal inflammation, exosome-mediated virulence factor dissemination to the liver, compounded gut microbiota dysbiosis, and convergent apoptosis across the pancreas, liver, and kidneys. Divergent arrows illustrate the temporal dissociation between bacterial load decline and persistent tissue injury. NAFLD: Non-alcoholic fatty liver disease; OMV: Outer membrane vesicles; IL: Interleukin; TNF-α: Tumor necrosis factor-alpha; LPS: Lipopolysaccharide; H. pylori: Helicobacter pylori.