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[Periapoptotic markers in children with Helicobacter pylori infection]
Aldona Kotłowska-Kmieć1, Alicja Bakowska, Ewa Wołowska
1Specjalistyczny ZOZ Nad Matka i Dzieckiem w Gdańsku, Oddział Interny Dzieci, 80-308 Gdańsk. akmiec@amg.gda.pl
Insights
Helicobacter pylori infection in children with chronic gastritis activates apoptosis, particularly via the Fas/FasL pathway. Fas receptor expression decreased after successful H. pylori eradication.
Area of Science:
- Gastroenterology
- Immunology
- Pediatrics
Background:
- Helicobacter pylori (Hp) infection is linked to chronic gastritis, affecting gastric mucosa cell metabolism and apoptosis.
- Apoptosis, or programmed cell death, plays a crucial role in maintaining tissue homeostasis and can be dysregulated in Hp infection.
- Periapoptotic markers like Fas, FasL, and Bcl-2 are key regulators of apoptosis.
Purpose of the Study:
- To investigate the relationship between periapoptotic markers (Fas, FasL, Bcl-2) and Hp infection in children with chronic gastritis.
- To determine the role of these markers in Hp-induced apoptosis and their changes following eradication therapy.
Main Methods:
- Study included 49 children with chronic abdominal pain, divided into groups with and without Hp infection, and a group post-eradication.
- Hp infection confirmed using four diagnostic methods.
- Gastric mucosa tissue samples analyzed via immunohistochemistry for Fas, FasL, and Bcl-2 expression.
Main Results:
- FasL and Bcl-2 expression were present in all children, regardless of Hp status.
- Fas receptor expression was significantly higher (p<0.05) in children with Hp infection compared to uninfected children.
- After successful H. pylori eradication, Fas and Bcl-2 expression significantly decreased (p<0.05).
Conclusions:
- Helicobacter pylori infection activates apoptosis in gastric mucosa, primarily through the Fas/FasL pathway.
- The Fas receptor shows a significant association with Hp infection and its expression is reduced post-eradication.
- These findings highlight the role of apoptosis markers in Hp-related gastritis in children.
Unlabelled:
Helicobacter pylori (Hp) infection influences cell metabolism and apoptosis in the epithelium and lymphocytes of gastric mucosa. It may cause difficulties in the elimination of bacteria and lead to chronic gastritis. THE AIM OF THE STUDY was to find if there is a relationship between periapoptotic markers such as Fas, FasL and Bcl-2 in gastric mucosa in children with chronic gastritis and with Hp infection.
Material And Methods:
Forty-nine children with chronic abdominal pain were included in the study. They, were divided into three groups: group I without Hp (22) group II with (27) Hp infection. Eleven children from the second group who had follow-up endoscopy after eradication therapy formed group III. Hp infection was confirmed by 4 different methods. The triple- drug treatment was applied. Tissue samples from the gastric mucosa were obtained, during upper gastrointestinal endoscopy, for microscopic evaluation (according to the Sydney classification) and immunohistochemistry. In the analysed groups the percentage of patients with periapoptotic markers (Fas, FasL, Bcl-2) was established. The Fas antigen was estimated by immunofluorescent and immunoenzymatic methods. The FasL I Bcl-2 receptors were evaluated by the immunoenzymatic method.
Results:
The expression of FasL and Bcl-2 receptors was found in all children without Hp infection. The expression of Fas antigen was less frequent in this group. The expression of Fas receptor was statistically significantly more frequent (p<0.05) in children with Hp infection. The expression of FasL and Bcl-2 in children with Hp infection was similar to group I (without Hp infection). In group of children after eradication treatment the expression of Fas and Bcl-2 (p<0.05) markers were significantly less frequent.
Conclusions:
Helicobacter pylori activates apoptosis by two pathways. It appears that the Fas/FasL pathway is the main one. Only in the case of Fas receptor there is a link between its significantly more frequent expression with Hp infection and its reduction after eradication treatment.
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