Ultrastructural study of Helicobacter pylori‐associated gastritis

Abstract

Endoscopic biopsies of antral mucosa from 26 patients with Helicobacter pylori-associated gastritis were studied by electron microscopy (EM). Scanning electron microscopy (SEM) showed clustering of H. pylori in the intercellular areas, being entrapped by the microvilli which were decreased at the sites where the bacilli were seen. The observations of SEM were confirmed by transmission electron microscopy (TEM), which showed adherence of the bacilli to the cell surface, producing cup-shaped depressions in the epithelial cells, and occasionally intracellular infiltration by H. pylori. There were also depletion of mucus granules, degenerative changes, and disruption of intercellular junction complexes of the epithelial cells. Post-treatment biopsies showed complete disappearance of the bacilli, and ultrastructural changes associated with H. pylori infection were resolved.

Modes of adherence of Helicobacter pylori to gastric surface epithelium in gastroduodenal disease: A possible sequence of events leading to internalisation

“…Thomsen et al (7) could demonstrate only loose attachment of the organisms and suggested that cell adherence is probably not an important virulence trait. In contrast, most other studies, using scanning or transmission electron microscopy, were able to show various forms of firm attachment between H. pylori and gastric cells, often resulting in deformation, blunting or focal ablation of gastric microvilli (8,12,15,17,23). This was comparable to, but possibly biochemically different from, the ''attaching-effacing'' effect observed with E. coli strains carrying the eae-gene (EPEC-strains; 12,17).…”

“…However, the results have often been discordant and in part difficult to interpret: different study models were applied, involving animal cells (14), cultured human gastric cells (9), gastric cancer cell lines (17, 21, 31), as well as tumour cell lines of other origin (18,19,22). Some investigations used live cells from patients with dyspepsia (3, 10) or gastritis (5,7,8,11,13), and only a few have included test materials from patients with gastric or duodenal ulcers (6,20). Studying adherence of H. pylori using cell lines, especially of non-gastric origin, has obvious limitations.…”

“…This was comparable to, but possibly biochemically different from, the ''attaching-effacing'' effect observed with E. coli strains carrying the eae-gene (EPEC-strains; 12,17). The specialised attachment sites on gastric cells were described as ''abutting'' (3,10), ''pedestal'' (8,11,12,24), or ''cup-like'' (8). However, some investigators failed to show such pedestal formations (4).…”

“…However, it must be noted that these investigators studied patients with dyspeptic symptoms without evidence of gastric or duodenal ulcer disease. Further studies revealed various modes of cell adhesion (3,(8)(9)(10)(11)(12) and according to some reports H. pylori was demonstrated in close proximity to parietal cells and even inside the canaliculi of resting (gastric) cells (4,8,10,13,14). …”

“…At the same time, however, Hazell et al (7) consistently observed penetration of the bacteria in the deep parts of the intercellular junctions. In contrast, many reports have demonstrated occasional (6,8,10,11,14,20,21) or frequent (12) internalisation of H. pylori in gastric mucous cells (8,10,11,14,20), parietal cells (4,14,20) or various cell lines (12,21,22). The intracellular organisms were mostly viable and sometimes associated with mucous droplets or granules (23) or vacuole spaces (22).…”