Medycyna wieku rozwojowego · 2009
[Periapoptotic markers in children with Helicobacter pylori infection].
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Kotłowska-Kmieć Aldona, Bakowska Alicja, Wołowska Ewa, Łuczak Grazyna, Liberek Anna
Аннотация
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.
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.