Antral gastric permeability to antigens in mice is altered by infection with Helicobacter felis

Citation
T. Matysiak-budnik et al., Antral gastric permeability to antigens in mice is altered by infection with Helicobacter felis, EUR J GASTR, 11(12), 1999, pp. 1371-1377
Citations number
27
Categorie Soggetti
Gastroenerology and Hepatology
Journal title
EUROPEAN JOURNAL OF GASTROENTEROLOGY & HEPATOLOGY
ISSN journal
0954691X → ACNP
Volume
11
Issue
12
Year of publication
1999
Pages
1371 - 1377
Database
ISI
SICI code
0954-691X(199912)11:12<1371:AGPTAI>2.0.ZU;2-J
Abstract
Objective Gastric inflammation is observed not only during Helicobacter pyl ori infection but also after eradication of the bacterium. The hypothesis t hat an altered gastric permeability could be involved was tested using a mo del of mice infected with Helicobacter felis, Design The antral and corpus gastric permeability during infection and afte r 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 i n Ussing chambers, and fluxes of sodium (JNa), mannitol (JMan) and horserad ish peroxidase (HRP) under intact (JHRPi) and degraded (JD) form were measu red, Results In healthy mice, JNa, JMan, JHRPi and JD, respectively, were greate r in the antrum (6.5 +/- 0.5 mu Eq/ h.cm(2); 0.137 +/- 0.016 mu mol/h.cm(2) ; 30.4 +/- 7.4 ng/h.cm(2) and 852 +/- 173 ng/h.cm(2)) than in the corpus (5 .0 +/- 0.3 mu Eq/ h.cm(2); 0.085 +/- 0.013 mu mol/h.cm(2); 9.5 +/- 2.8 ng/h .cm(2) and 434 +/- 139 ng/h,cm(2)), In H. felis-infected mice, HRP fluxes i n the antrum were increased (JHRPi =182 +/- 86, JD = 948 +/- 94 ng/h.cm(2)) as compared to controls (JHRPi = 10.3 +/- 2.6, JD = 458 +/- 98 ng/h.cm(2)) , Bacterial eradication led to the reduction of intact (JHRPi = 53 +/- 26 n g/h.cm) but not of degraded (JD = 844 +/- 213 ng/h.cm) HRP fluxes. After er adication, degraded HRP fluxes returned to normal in mice without inflammat ion (JD = 558 +/- 36 ng/h.cm(2)) but not in those with persistent inflammat ion (JD = 987 +/- 310 ng/h.cm(2)). Conclusions The results suggest that during H. felis infection, bacterial c olonization and inflammation lead to an increased gastric permeability alon g the direct and degradative pathways, respectively, Such an increased anti genic load could contribute to the perpetuation of gastric inflammation aft er bacterial eradication, and possibly to food protein sensitization, Eur J Gastroenterol Hepatol 11:1371-1377 (C) 1999 Lippincott Williams & Wilkins.