Helicobacter pylori alters exogenous antigen absorption and processing in a digestive tract epithelial cell line model

To study the influence of Helicobacter pylori on epithelial barrier functio n, bacteria, bacterial sonicates, or broth culture supernatants were incuba ted for 24 h with HT29-19A intestinal cells grown as monolayers. Subsequent ly, the monolayers were mounted in Ussing chambers, and electrical resistan ce (R), fluxes of Na-22 (JNa) and C-14 mannitol (JMan) (markers of the para cellular pathway), and fluxes of horseradish peroxidase (HRP) in total (J(3 )H-HRP), intact (JHRPi), and degraded forms were measured. H. pylori did no t induce any modification of the paracellular pathway (R = 148 +/- 10 versu s 174 +/- 16 Omega . cm(2); JNa = 4.16 +/- 0.44 versus 3.51 +/- 0.41 mu Eq/ h cm(2); JMan = 0.081 +/- 0.01 versus 0.058 +/- 0.009 mu mol/h cm(2)), nor did it modify J(3)H-BRP (2,201 +/- 255 versus 2,110 +/- 210 ng/h . cm(2) fo r H. pylori-infected and control cells, respectively). However, in the pres ence of H. pylori, we observed a significant increase in JHRPi (520 +/- 146 versus 171 +/- 88 ng/h . cm(2)). This effect was not dependent of the cag status of the strain and was not reproduced by the sonicates or the culture supernatants. It was related to the presence of urease, since a urease-neg ative mutant of H. pylori did not induce this effect. Ammonia and bafilomyc in A(1), two agents known to increase the endolysosomal pH, reproduced the increase in JHRPi In conclusion,H. pylori does not affect directly the inte grity of intercellular junctions of epithelial cells in vitro, but it incre ases the passage of intact HRP, probably by inhibition of the intralysosoma l degradation due to the release of ammonia. The increased transport of int act macromolecules may contribute to the induction and maintenance of gastr ic inflammation by H. pylori.