||Background: Helicobacter pylori infection results in a cascade of biochemical events in the
gastric mucosa. In the inflammatory process, mast cells play a pivotal role as initiators and regulators of inflammation. As they play a key role in infection and immunity and because they are present in large numbers in the mucosa of the gastrointestinal tract, it is likely that mast cells participate in the pathophysiology of Helicobacter pylori associated gastroduodenal diseases. Aims & Methods: Our paper tried to investigate by ultrastructural examination the role of mast cells in the pathophysiology of H. pyloriassociated gastritis. The study comprised 56 H. pylori-positive and 20 H. pylori-negative patients. During endoscopy, gastric antral and body biopsies were taken for the assessment of H. pylori and morphological examination. All samples were evaluated according to the Sydney system and mast cell density in both the corpus and antrum mucosa was analyzed by modified Romanovsky stain. Wilcoxon Matched Pairs test was used to determine the relationship between mast cells and other histopathological parameters. The mast cell density between H. pylori positive and negative groups was compared by Student test. The specimens from 12 infected patients were processed for ultrastructural examination, contrasted with acetate-uranyl and leadcitrate
and studied with a JEM-1010 electron microscope. Results: In our study, mast cell density was
similar in the corpus and antral mucosa (p > 0.5) but higher in the HP-positive group than in the HP-negative group (p < 0.01), both in the antrum and corpus. At the same time we observed that there was a direct correlation between the mast cell infiltration and the increased activity of the gastritis, as well as between the mast cell infiltration and HP density in the antrum and corpus (p < 0.005). There was no correlation between the mast cell infiltration and intestinal metaplasia or between the mast cell infiltration and gastric atrophy (p>0, 05). At the ultrastructural examination, we found many mast cells within the lamina propria of the H. pylori-positive subjects. In no infected patients the mast cells were normal, with regular shape nucleus and electron dense granules in the cytoplasm from the lamina propria of the antrum and corpus mucosa. The majority of the mast cells were present in sub epithelial areas, around blood vessels, in the vicinity of
eosinophils and rarely around nerves. Hence, it is strongly suggested that the mast cells infiltrating the inflamed mucosa are activated and may induce tissue damage. Conclusion: All of the above supported the fact that mast cells play a role in the occurrence and development of the pathogenesis of HP infection. Mast cells can penetrate the basal membrane and move toward the interepithelial space. During this process, degranulation appears gradually, which results in the phenomena of vacuolation.The relationship between mast cells and HP infection and the effect of the mediators secreted by mast cells on the pathophysiology of HP associated gastritis needs further investigation. Thus, manipulating mast-cell adhesion may be an important strategy for controlling the outcome of the inflammatory response.
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