Gastric Helicobacter infection inhibits development of oral tolerance to food antigens in mice.

The increase in the transcellular passage of intact antigens across the digestive epithelium infected with Helicobacter pylori may interfere with the regulation of mucosal immune responses. The aim of this work was to study the capacity of Helicobacter infection to inhibit the development of oral tolerance or to promote allergic sensitization and the capacity of a gastro-protective agent, rebamipide, to interfere with these processes in mice. Oral tolerance to ovalbumin (OVA) was studied in 48 C3H/He 4-week-old mice divided into four groups: (i) OVA-sensitized mice; (ii) OVA-"tolerized" mice (that is, mice that were rendered immunologically tolerant); (iii) H.

Colonization of gnotobiotic mice with human gut microflora at birth protects against Escherichia coli heat-labile enterotoxin-mediated abrogation of oral tolerance.

Previous work has shown that the indigenous gut microflora in mice plays a protective role against Escherichia coli heat-labile enterotoxin (LT)-mediated abrogation of oral tolerance to an unrelated co-ingested protein. To assess potential protection by human gut microflora, we studied the effect of human gut microflora in a murine model. Oral tolerance was studied in adult gnotobiotic mice (i.