title: The role of luminal factors in the recovery of gastric function and behavioral changes after chronic Helicobacter pylori infection.
abstract: 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 mo and then treated with antibiotics or placebo for 2 wk. Gastric emptying was measured using videofluoroscopy, feeding behavior using a 24-h feeding system, and intestinal permeability using an isolated jejunal segment arterially perfused with an artificial oxygen carrier, hemoglobin vesicles. Immune responses were assessed by CD3(+) cell counts and anti-Hp antibodies using ELISA. To determine the role of luminal factors in host physiology posteradication, groups of mice received the probiotics containing Lactobacillus rhamnosus R0011 and L. helveticus R0052 or placebo for 2 wk or crude Hp antigen weekly for 2 mo. 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 posteradication. 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, influences 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.
authors.affiliation: McMaster Univ. HSC 3N49C, 1200 Main St. West, Hamilton, Ontario, Canada. verdue@mcmaster.ca
authors.forename: Elena F
authors.initials: EF
authors.lastname: Verdu
authors.forename: Premysl
authors.initials: P
authors.lastname: Bercik
authors.forename: Xian Xi
authors.initials: XX
authors.lastname: Huang
authors.forename: Jun
authors.initials: J
authors.lastname: Lu
authors.forename: Nafia
authors.initials: N
authors.lastname: Al-Mutawaly
authors.forename: Hiromi
authors.initials: H
authors.lastname: Sakai
authors.forename: Thomas A
authors.initials: TA
authors.lastname: Tompkins
authors.forename: Kenneth
authors.initials: K
authors.lastname: Croitoru
authors.forename: Eihun
authors.initials: E
authors.lastname: Tsuchida
authors.forename: Mary
authors.initials: M
authors.lastname: Perdue
authors.forename: Stephen M
authors.initials: SM
authors.lastname: Collins
mesh_terms: D000818:Animals; D000942:Antigens, Bacterial / Q000032:analysis; D002908:Chronic Disease; D004415:Dyspepsia / Q000628:therapy; D005247:Feeding Behavior; D005746:Gastric Emptying / Q000502:physiology; D005756:Gastritis / Q000209:etiology; D016481:Helicobacter Infections / Q000188:drug therapy / Q000503:physiopathology*; D016480:Helicobacter pylori / Q000276:immunology; D052198:Lactobacillus helveticus; D052201:Lacticaseibacillus rhamnosus; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D019936:Probiotics / Q000627:therapeutic use; D013270:Stomach / Q000382:microbiology / Q000503:physiopathology*
chemical_list: D000942:Antigens, Bacterial