Helicobacter pylori energy metabolism

Helicobacter pylori energy metabolism refers to the specialized biochemical pathways, including the Entner-Doudoroff pathway and a non-cyclic tricarboxylic acid (TCA) cycle, that the bacterium uses to survive in the human stomach [1, 7]. Key enzymes such as pyruvate:ferredoxin oxidoreductase (PFOR) and fumarate reductase are essential for ATP production and redox balance under microaerophilic conditions [1, 4]. These metabolic pathways are distinct from those in humans, making them attractive therapeutic targets for eradicating H. pylori infections [1, 12]. Drugs like nitazoxanide and bismuth-based compounds act by inhibiting PFOR or disrupting electron transport, thereby halting bacterial growth [1, 11]. Additionally, H. pylori infection induces metabolic reprogramming in host gastric cells, promoting glycolysis and contributing to the development of gastric cancer [2, 3, 13]. Targeting these metabolic vulnerabilities is a promising strategy to overcome the challenge of increasing antibiotic resistance in clinical strains [11, 12].

Other names

Helicobacter pylori metabolic pathwaysH. pylori bioenergeticsHelicobacter pylori intermediary metabolism

Inhibition of key metabolic enzymes such as pyruvate:ferredoxin oxidoreductase (PFOR), disruption of the electron transport chain, and inhibition of fumarate reductase to halt ATP production and redox balance [1, 11].