Accelerated biological aging mediates the association between inflammatory markers with Helicobacter pylori infection and mortality

The aim of this study was to explore the systemic inflammation response in relation to mortality in Helicobacter pylori (H. pylori) infection, and whether this relationship was mediated by accelerated biological aging. This cross-sectional study encompassed U.S. participants from National Health and Nutrition Examination Survey (NHANES) in 1999–2000. Kaplan-Meier survival curve, Cox regression analysis, K-means clustering, mediation analysis and restricted cubic spline (RCS) were used to explore the relationships between inflammatory markers, biological aging, H. pylori infection and all-cause mortality. A total of 3509 U.S. participants enrolled form NHANES 1999–2000. Compared with H. pylori seronegative participants, H. pylori seropositive participants had significantly higher all-cause mortality (P < 0.001). Among these H. pylori seropositive participants, both phenotypic age acceleration (PhenoAgeAccel) and all-cause mortality were positively associated with the increased levels of inflammation (P < 0.001). A significant indirect effect of inflammatory markers (neutrophil count and systemic inflammatory response index (SIRI)) with H. pylori infection on all-cause mortality through PhenoageAccel was found, and the proportions mediated were 50.0% and 49.1%, respectively. The elevation of blood inflammatory markers is positively associated with an increased risk of all-cause mortality in H. pylori infection among U.S. population, and accelerated biological aging might be one of its biological mechanisms.