The role of chronic infections, such as Helicobacter pylori (Hp), to produce sustained changes in host physiology remains controversial. In this study we investigate whether the antigenic or bacterial content of the gut, after Hp eradication, influences the changes in gut function induced by chronic Hp infection. Mice were infected with Hp for 4 months and then treated with antibiotics or placebo for 2 weeks. Gastric emptying was measured using videofluoroscopy, feeding behavior using a 24-hour feeding system and intestinal permeability using an isolated arterially perfused jejunal segment. Immune responses were assessed by CD3⁺ cell counts and anti-Hp antibodies using ELISA. To determine the role of luminal factors in host physiology post eradication, groups of mice received the probiotics containing L. rhamnosus R0011 and L. helveticus R0052 or placebo for 2 weeks, or crude Hp antigen weekly for 2 months. Chronic Hp infection was associated with delayed gastric emptying, increased intestinal permeability, and increased gastric CD3⁺ cell counts. Hp-induced altered feeding patterns did not reverse after eradication. Probiotics accelerated the recovery of paracellular permeability and delayed gastric emptying, improved the CD3⁺ cell counts, and normalized altered feeding patterns post-eradication. Hp antigen resulted in increased anti-Hp antibodies and increased CD3⁺ cell counts in the stomach and delayed recovery of gastric function. Our results suggest that the bacterial content of the gut, as well as the presence of relevant antigens, influence the rate of recovery of host pathophysiology induced by chronic Hp infection. These changes do not seem to occur in association with modulation of intestinal permeability.