Adhesion of Helicobacter pylori to gastric epithelial cells in primary cultures obtained from stomachs of various animals

Abstract

Of 35 strains of Helicobacter pyloni tested, 5 were found to adhere well to HEp-2 cells. We selected three of these adhesive strains and four from the remaining strains to examine their ability to adhere to gastric epithelial cells in primary cultures obtained by collagenase digestion of stomachs from mice, rats, Mongolian gerbils, guinea pigs, pigs, and cynomolgus monkeys. The three adhesive strains adhered well to epithelial cells from monkey and pig gastric antra. The adhesion was inhibited by incubating the bacterial cells with fetuin, and this inhibition was further confirmed by the binding of gold-labeled fetuin to the surface of the adhesive strains. However, these adhesive strains only weakly adhered to fundic epithelial cells from monkeys and pigs and to gastric epithelial cells from the other animals. As for the four strains poorly adhesive to HEp-2 cells, they adhered weakly to gastric epithelial cells from all of the animals tested. They had higher hemagglutination titers than the adhesive strains, showing that there was no correlation between hemagglutination titers and the ability to adhere to gastric cells. Taking the similarities of human and monkey or pig stomachs into consideration, these results suggest that the primary target cell of H. pylon in colonization in human stomachs is the antral epithelial cell and that the putative adhesin involved in adhesion has affinity for fetuin.

Helicobacter pylori Disrupts Epithelial Barrier Function in a Process Inhibited by Protein Kinase C Activators

“…Our results showed that H. pylori sonicates produced a dramatic decrease in TER in T84 monolayers and induced a rapid increase in [ 14 C]mannitol flux not only across the T84 model epithelium but also across the rat mucosa. These data suggest that the bacterium can alter the barrier function of the epithelium without adhering to it, as it is known that H. pylori does not bind to rat gastric epithelial cells (29) and that the adhesion of this bacterium to T84 cells is maximal at pH 5.4 (10), while our experiments were carried out under neutral pH conditions. Bacterial sonicates fail to produce any effect in the TER of MDCK cells (data not shown), which are also able to establish monolayers with physiological resistance.…”

Inhibition of Helicobacter pylori binding to gastrointestinal epithelial cells by sialic acid-containing oligosaccharides

“…Bacteria are generally most numerous in the antrum but are also found bound to patches of gastric metaplasia in the duodenum and the esophagus (5). The localized adherence of H. pylori to gastric epithelial cells as well as their apparent selectivity for the antrum (30) suggests that the organism specifically recognizes epithelial cell surface constituents. Based on hemagglutination and cell binding experiments, H. pylori was proposed to recognize 3Ј-sialyllactose (NeuAc␣2-3Gal␤1-4Glc; 3ЈSL) (13,15).…”

Helicobacter pyloricytotoxin VacA increases alkaline secretion in gastric epithelial cells

“…Studies in the whole intact epithelium. Hp resides within the mucus layer or is anchored to the luminal surface by means of the adhesines (3,18,27,28). Hence, VacA toxin is presumably released by the bacterium directly onto the apical cell membrane.…”