Helicobacter pylori and gastric inflammation (original) (raw)
Related papers
Gastric mucosal response to Helicobacter pylori
The Keio Journal of Medicine, 2002
Since Marshall's discovery before 20 years, Helicobacter pylori (H. pylori) infection is re portedly to be associated with a variety of clinical outcomes including peptic ulcer disease and gastric cancer. The first step of the H. pylori colonization might be its adhesion to the surface epithelial cells, which evokes gastric inflammatory events initiated by neutrophil recruitment from the microcircula tion. Mongolian gerbil is one of the suitable animal models for H. pylori infection, which exerts gastric ulcer and cancer with its bacterial infection. In H. pylori-colonized gerbils, extensive levels of micro vascular leukocyte adhesion and migration into the parenchymal side and significant levels of inflam matory cell infiltration are encountered. Bacterial urease not only neutralizes gastric luminal acid, but also plays as an adhesion factor to the surface epithelium. Recently, such an adhesion to the epithelium is reported to be important for bacterial type IV secretory system, which intermediates Cag A injection into the epithelial cells. Then, multiple chemokine and cytokine networks are activated and mucosal inflammatory lesion formation would be completed. In the long-term colonization of H. pylori, gastric mucosal cell turnover would be modified due to persistent inflammation and then such deregulation of cell turnover might link to the precancerous lesion formation.
How Does Helicobacter pylori Cause Mucosal Damage? Its Effect on Acid and Gastrin Physiology
Gastroenterology, 1997
Helicobacter pylori infection increases gastric acid secretion in patients with duodenal ulcers but diminishes acid output in patients with gastric cancer and their relatives. Investigation of the basic mechanisms may show how H. pylori causes different diseases in different persons. Infection of the gastric antrum increases gastrin release. Certain cytokines released in H. pylori gastritis, such as tumor necrosis factor a and specific products of H. pylori, such as ammonia, release gastrin from G cells and might be responsible. The infection also diminishes mucosal expression of somatostatin. Exposure of canine 0 cells to tumor necrosis factor a in vitro reproduces this effect. These changes in gastrin and somatostatin increase acid secretion and lead to duodenal ulceration. But the acid response depends on the state of the gastric corpus mucosa. The net effect of corpus gastritis is to decrease acid secretion. Specific products of H. pylori inhibit parietal cells. Also, interleukin 113, which is
Adherence of Helicobacter pylori to gastric epithelial cells and mucosal inflammation
Journal of Laboratory and Clinical Medicine, 2002
Adherence of Helicobacter pylori to the gastric epithelium is believed to be an important step in the induction of active inflammation of the mucosal layer. However, structural evidence showing a quantitative relationship between the adherence of H. pylori and severity of gastric mucosal inflammation is lacking. We therefore investigated the correlations between severity of gastritis and adherence of morphologically different forms of H. pylori. Fifty-seven biopsy specimens from the gastric bodies of patients with H. pylori-induced gastritis were examined. The severity of gastritis and the adherence and structure of H. pylori were determined with the use of light and scanning electron microscopy. We also investigated the ability of H. pylori organisms with different structural features to induce interleukin-8 secretion by human gastric adenocarcinoma (AGS) cells in vitro because production of interleukin-8 is related to H. pylori-associated gastritis. Furthermore, serum pepsinogen concentrations and cytotoxin-associated protein status in relation to adherence of H. pylori to the epithelial surface were examined. The results indicated that H. pylori organisms, which adhered firmly to the epithelial surface, were consistently long, tightly coiled bacilli. Histologically, those gastric mucosa samples with H. pylori firmly attached showed severe gastritis. H. pylori bacilli of greater length induced higher levels of interleukin-8 secretion. The serum pepsinogen I/II ratio showed a significant negative correlation with the grade of H. pylori adhesion (r ؍ ؊0.401, P < .01). We also noted a significant correlation between cytotoxinassociated protein status and the adherence of H. pylori (r ؍ 0.344, P < .05). A quantitative correlation was found between adherence of H. pylori and gastric inflammation. Both adherence and the induction of inflammation were found to be related to the structure of H. pylori. (J Lab Clin Med 2002;139:244-50) Abbreviations: CagA ϭ cytotoxin-associated protein; ELISA ϭ enzyme-linked immunosorbent assay
Effect of Helicobacter pylori on gastric epithelial cells
World Journal of Gastroenterology, 2014
Core tip: Helicobacter pylori (H. pylori ) is a gram negative bacterium that colonizes the gastric epithelium of more than half of the humankind. H. pylori use the gastric epithelial cells to manipulate the immune system to favor their survival and proliferation. In this review article, we focused on the mechanisms that facilitate the interaction between H. pylori and gastric epithelial cells, such as adhesion molecules, and we summarized the array of highly relevant outcomes of this interaction for the host.
Canadian journal of gastroenterology = Journal canadien de gastroenterologie, 2005
Infection of the human stomach with Helicobacter pylori may develop into gastritis, ulceration, adenocarcinoma and mucosal lymphomas. The pathogenic mechanisms that determine the clinical outcome from this microbial-epithelial interaction remain poorly understood. An increasing number of reports suggests that disruptions of epithelial barrier function may contribute to pathology and postinfectious complications in a variety of gastrointestinal infections. The aim of this review is to critically discuss the implications of H pylori persistence on gastric disease, with emphasis on the role of myosin light chain kinase, claudins and matrix metalloproteinases in gastric permeability defects, and their contribution to the development of cancer. These mechanisms and the associated signalling events may represent novel therapeutic targets to control disease processes induced by H pylori, a microbial pathogen that colonizes the stomach of over 50% of the human population.
Infection and Immunity, 2013
Helicobacter pylori infection of the stomach is related to the development of diverse gastric pathologies. The ability of H. pylori to compromise epithelial junctional complexes and to induce proinflammatory cytokines is believed to contribute to pathogenesis. The purpose of this study was to use an in vitro human gastric epithelial model to investigate the ability of H. pylori to affect permeability and the extent and polarity of the host inflammatory response. NCI-N87 monolayers were cocultured with live or heat-killed H. pylori or culture supernatants. Epithelial barrier function was measured by transepithelial electric resistance (TEER) analysis, diffusion of fluorescein isothiocyanate (FITC)-labeled markers, and immunostaining for tight junction proteins. Supernatants from both apical and basolateral chambers were tested for cytokine production by multiplex analysis.
Molecular response of gastric epithelial cells to Helicobacter pylori-induced cell damage
Cellular Microbiology, 1999
Infection with the Gram-negative bacterium Helicobacter pylori leads to different clinical and pathological outcomes in humans, including chronic gastritis, peptic ulcer disease and adenocarcinoma of the stomach. H. pylori-induced damage to gastric mucosal cells is controlled by bacterial virulence factors encoded by genes of the cag pathogenicity island, which trigger the in¯ammatory response of the host through the activation of nuclear factor kB-dependent gene transcription. Also, H. pylori infection impairs the processes of gastric mucosal healing through inhibition of epidermal growth factor receptor-dependent signal transduction pathways and induction of apoptosis. H. pylori infection may in¯uence the progression from chronic gastritis to gastric adenocarcinoma by stimulating cell proliferation and growth factor expression, inhibiting apoptosis and increasing the DNA mutation rate of infected gastric mucosa.
Epithelial damage by Helicobacter pylori in gastric ulcers
Histopathology, 1991
Epithelial damage by HeIicobacter pylori in gastric ulcers On review of 136 consecutive biopsies of benign gastric ulcer, Helicobacterpylori was detected in 78 cases (5 7.3%). The gastric epithelium colonized by Helicobacter pylori showed a characteristic constellation of changes, including loss of apical mucous portion of individual cells, drop-out of epithelial cells, epithelial pits, erosions and cellular tufts, indicative of cellular injury and regeneration. Among the 5 8 Helicobacter-negative cases, similar changes were not observed in the ulcer edges, except for two cases which exhibited some cellular tufts. Thus, the topographic association of Helicobacter pylori with epithelial damage in the gastric ulcer edges in more than half of the cases suggests that this organism probably plays an aetiological role in ulcerogenesis, at least in these cases. Furthermore, the epithelial changes are so distinctive that they can serve as a helpful histological indicator for the presence of Helicobacterpylori in gastric biopsies.