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The gastric pathogen  Helicobacter pylori  utilize glucose during metabolism, but the underlying mechanisms linking to oxygen-18 ( 18 O) and carbon-13 ( 13 C)-isotopic fractionations of breath CO 2  during glucose metabolism are poorly understood. Using the excretion dynamics of  18 O/ 16 O and  13 C/ 12 C-isotope ratios of breath CO 2 , we found that individuals with  Helicobacter pylori  infections exhibited significantly higher isotopic enrichments of  18 O in breath CO 2  during the 2h-glucose metabolism regardless of the isotopic nature of the substrate, while no significant enrichments of  18 O in breath CO 2  were manifested in individuals without the infections. In contrast, the  13 C-isotopic enrichments of breath CO 2  were significantly higher in individuals with  Helicobacter pylori  compared to individuals without infections in response to  13 C-enriched glucose uptake, whereas a distinguishable change of breath  13 C/ 12 C-isotope ratios was also evident when  Helicobacter pylori  utilize natural glucose. Moreover, monitoring the  18 O and  13 C-isotopic exchange in breath CO 2  successfully diagnosed the eradications of  Helicobacter pylori  infections following a standard therapy. Our findings suggest that breath  12 C 18 O 16 O and  13 C 16 O 16 O can be used as potential molecular biomarkers to distinctively track the pathogenesis of  Helicobacter pylori  and also for eradication purposes and thus may open new perspectives into the pathogen’s physiology along with isotope-specific non-invasive diagnosis of the infection.

Mechanisms linking metabolism of Helicobacter pylori to 18O and 13C-isotopes of human breath CO2