title: Antral gastric permeability to antigens in mice is altered by infection with Helicobacter felis.
abstract: OBJECTIVE
  Gastric inflammation is observed not only during Helicobacter pylori infection but also after eradication of the bacterium. The hypothesis that an altered gastric permeability could be involved was tested using a model of mice infected with Helicobacter felis.
  
  
  METHODS
  The antral and corpus gastric permeability during infection and after eradication of bacteria was studied.
  
  
  METHODS
  Gastric fragments from the antrum and corpus of healthy mice, mice infected with H. felis, or mice after bacterial eradication, were mounted in Ussing chambers, and fluxes of sodium (JNa), mannitol (JMan) and horseradish peroxidase (HRP) under intact (JHRPi) and degraded (JD) form were measured.
  
  
  RESULTS
  In healthy mice, JNa, JMan, JHRPi and JD, respectively, were greater in the antrum (6.5 +/- 0.5 microEq/h.cm2; 0.137 +/- 0.016 micromol/h.cm2; 30.4 +/- 7.4 ng/h.cm2 and 852 +/- 173 ng/h.cm2) than in the corpus (5.0 +/- 0.3 microEq/h.cm2; 0.085 micro 0.013 micromol/h.cm2; 9.5 +/- 2.8 ng/h.cm2 and 434 +/- 139 ng/h.cm2). In H. felis-infected mice, HRP fluxes in the antrum were increased (JHRPi = 182 +/- 86, JD = 948 +/- 94 ng/h.cm2) as compared to controls (JHRPi = 10.3 +/- 2.6, JD = 458 +/- 98 ng/h.cm2). Bacterial eradication led to the reduction of intact (JHRPi = 53 +/- 26 ng/h.cm) but not of degraded (JD = 844 +/- 213 ng/h.cm) HRP fluxes. After eradication, degraded HRP fluxes returned to normal in mice without inflammation (JD = 558 +/- 36 ng/h.cm2) but not in those with persistent inflammation (JD = 987 +/- 310 ng/h.cm2).
  
  
  CONCLUSIONS
  The results suggest that during H. felis infection, bacterial colonization and inflammation lead to an increased gastric permeability along the direct and degradative pathways, respectively. Such an increased antigenic load could contribute to the perpetuation of gastric inflammation after bacterial eradication, and possibly to food protein sensitization.
authors.affiliation: INSERM E9925, Faculté Necker, Paris, France. matysiak@necker.fr
authors.forename: T
authors.initials: T
authors.lastname: Matysiak-Budnik
authors.forename: K
authors.initials: K
authors.lastname: Hashimoto
authors.forename: M
authors.initials: M
authors.lastname: Heyman
authors.forename: A
authors.initials: A
authors.lastname: de Mascarel
authors.forename: J F
authors.initials: JF
authors.lastname: Desjeux
authors.forename: F
authors.initials: F
authors.lastname: Mégraud
mesh_terms: D000818:Animals; D000941:Antigens / Q000378:metabolism*; D001692:Biological Transport; D005753:Gastric Mucosa / Q000166:cytology / Q000378:metabolism* / Q000382:microbiology; D005756:Gastritis / Q000209:etiology; D016998:Helicobacter / Q000302:isolation & purification; D016481:Helicobacter Infections / Q000378:metabolism* / Q000382:microbiology; D051379:Mice; D008810:Mice, Inbred C57BL; D010539:Permeability; D011706:Pyloric Antrum / Q000378:metabolism / Q000382:microbiology; D014510:Urease / Q000378:metabolism
chemical_list: D000941:Antigens; D014510:Urease