Background/Aim: Bacterial infection can trigger the development of functional GI disease. Here we investigate the role of the gut-brain axis in gastric dysfunction during and after chronic H. pylori infection. Methods: Control and chronically H. pylori infected Balb/c mice were studied before and two months after bacterial eradication. Gastric motility and emptying were investigated using videofluoroscopy image analysis. Gastric mechanical viscerosensitivity was assessed by cardioautonomic responses to distension. Feeding patterns were recorded by a computer-assisted system. Plasma leptin, ghrelin and CCK levels were measured using ELISA. IL-1, TNF-, POMC and NPY mRNAs were assessed by in situ hybridizations on frozen brain sections. Gastric inflammation was assessed by histology and immunohistochemistry. Results: H. pylori infected mice ate more frequently than controls but consumed less food per bout, maintaining normal body weight. Abnormal feeding behavior was accompanied by elevated plasma ghrelin and postprandial CCK, higher TNF- (median eminence) and lower POMC (arcuate nucleus) mRNA. Infected mice displayed delayed gastric emptying and visceral hypersensitivity. Eradication therapy normalized gastric emptying, improved gastric sensitivity but had no effect on eating behavior. This was accompanied by persistently increased TNF- in the brain and gastric CD3⁺ T cell counts. Conclusions: Chronic H. pylori infection in mice alters gastric emptying and mechanosensitivity that improve after bacterial eradication. A feeding pattern reminiscent of early satiety persists after H. pylori eradication and is accompanied by increased TNF- in the brain. The results support a role for altered gut-brain pathways in the maintenance of post-infective gut dysfunction.