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Introduction: Acute gastritis resulting from H. pylori infections is of great importance given its tendency to become chronic and its premalignant nature. The present study aimed to find relationship between the changes in the number of gastric mucosal stem cells and H. pylori infection in the stomach.
Materials and Methods: The total of 50 patient’s stomach biopsies, aged 35 to 45 who admitted to hospital with dyspeptic complaints was used for study. The patients with comorbidities such as asthma, advanced hepatic and renal diseases and bleeding disorders, peptic ulcers, a history of malignancy, gastrointestinal system surgery, gastrointestinal system bleeding, received H. pylori treatment, non-steroid anti-inflammatory drugs or opioids and also proton pump inhibitors were excluded. 25 of 50 people were positive H. pylori, and the remaining 25 were negative. The specimens were stained with Musashi-1, CD44, CD105, CD29 for detection of some of GSC and also NfKB for detecting inflammatory reaction and p53 for evaluate genome destruction. Immunopositive cells were counted under a light microscope and then analyzed.
Results: The assessment revealed a significantly increased in the number of gastric GSC markers and CD44 (+) stem cells, (p=0.000) which define as a cancer stem cell marker, in H. pylori (+) patients, compared to a significantly decreased number of CD105, CD29, and Musashi-1 (+) cells (p=0.000). There were no p53 expression in both groups, but expression of NfKB were decreased in H.pylori (+).
Conclusions: The findings suggest that H. pylori impair the histophysiological structure of gastric mucosa by increasing the CD44 expression and decreasing the number of CD105, CD29, Musashi-1 (+) stem cells and NfKB expression and sets the ground for gastric malignancies by becoming a chronic infection through adverse effects on tissue reparation and regeneration.
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