Bacterial adhesion and disease activity in Helicobacter associated chronic gastritis.

Abstract

Ultrastructural examination of biopsies showing Helicobacter pylon associated chronic gastritis reveals close attachment between gastric surface epithelial celis and the organism. The finding of 'adhesion pedestals', which represents a cellular response to the presence of the organism, is analogous to the response ofintestinal cells to enteropathogenic E coli. Thus the development of bacterial attachment sites in H pylori associated gastritis might be an indication of pathogenicity. We have therefore explored the relationship between the proportion of organisms forming attachment sites and histological indices of disease 'activity'. Antral biopsies from 40 patients with Hpyloni positive gastritis were examined histologically and ultrastructurally, and the percentage of attached organisms compared with subjective assessments of epithelial degeneration, mucin depletion, polymorphonuclear and chronic inflammatory cell infiltration. We found a significant increase in the proportion of attached bacteria in cases showing histological epithelial degeneration, and a significant decrease in cases showing intraepithelial polymorph infiltration. The direct relationship between bacterial attachment and cellular degeneration lends further support to a pathogenic effect. Reduced attachment in the face of polymorph infiltration might indirectly reflect aspects of the immune responsenamely, blocking of adhesion by IgA, with complement activation and generation of leucotactic factors.

Helicobacter pylori-Induced Chronic Active Gastritis, Intestinal Metaplasia, and Gastric Ulcer in Mongolian Gerbils

“…In the human stomach, H. pylori was first described to adhere to the apical surface of the surface mucous cells, 20 and its ability to adhere was considered an essential factor for the stable infection by H. pylori. 21 In addition, several studies using in vitro experimental systems have suggested that this attachment accelerates the production of interleukin-8, which induces neutrophil infiltration. 22,23 In the human stomach, as shown by Shimizu et al, 24 this organism actively col-onizes not only the apical surface but also the SMGL.…”

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

“…Thus, the presence of different cell adherence forms of H. pylori has been correlated with cytolysis and disintegration/destruction of the gastric epithelium (3,11,13). Another feasible indirect mechanism of action is the recruitment and activation of inflammatory cascade(s) with potent chemokines (15).…”

“…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, some investigators failed to show such pedestal formations (4). On the other hand, it was noted that more than one adhesion form could be encountered within the same biopsy material and sometimes an individual H. pylori organism displayed several adhesion forms simultaneously (3,10,12;Figs. 4 & 5).…”

“…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). …”