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Helicobacter pylori gastritis in children is associated with a regulatory T-cell response
Paul R Harris1, Shelton W Wright, Carolina Serrano
1Department of Pediatrics, Pontificia Universidad Católica de Chile and Hospital Dr. Sótero del Río, Santiago, Chile.
Insights
Children infected with Helicobacter pylori show less gastric inflammation and more T regulatory (Treg) cells. These Treg cells may protect children from H pylori-induced stomach issues.
Area of Science:
- Gastroenterology
- Immunology
- Pediatrics
Background:
- Helicobacter pylori infection commonly causes gastritis but infrequently leads to ulcers in children.
- T regulatory (Treg) cells are known to suppress T-cell-mediated inflammation, a key factor in H pylori-induced gastritis in adults.
Purpose of the Study:
- To investigate and compare gastric histopathology and Treg cell responses in H pylori-infected children and adults.
Main Methods:
- Prospective evaluation of gastric tissue from 36 children and 79 adults in Santiago, Chile.
- Assessed H pylori presence, Sydney classification histopathology, and Treg responses via immunoassay, immunohistochemistry, and real-time PCR.
Main Results:
- H pylori infection rates were similar (50% in children, 65% in adults).
- Children exhibited significantly reduced gastritis (P < .05) compared to adults.
- H pylori-infected children had increased gastric Treg cells and elevated Treg cytokines (TGF-β1, IL-10) (P < .03, P < .05).
Conclusions:
- Gastric pathology is diminished in H pylori-infected children relative to adults.
- Increased local Treg cell responses in children appear to down-regulate H pylori-induced inflammation and ulceration.
Background & Aims:
Helicobacter pylori infection in children infrequently causes gastroduodenal mucosal ulceration. Because H pylori induces T-cell dependent gastric inflammation in adults and T regulatory (Treg) cells suppress T-cell-dependent pathology, we evaluated gastric histopathology and Treg cell responses in H pylori-infected children and adults.
Methods:
Gastric tissue from 36 children and 79 adults with abdominal symptoms in Santiago, Chile, was evaluated prospectively for H pylori bacteria and histopathology using the Sydney classification and Treg responses using immunoassay, immunohistochemistry, and real-time polymerase chain reaction.
Results:
Eighteen (50%) of the children and 51 (65%) of the adults were infected with H pylori. Children and adults were colonized with similar levels of H pylori. However, the level of gastritis in the children was reduced substantially compared with that of the adults (P < .05). Coincident with reduced gastric inflammation, the number of Treg cells and levels of Treg cytokines (transforming growth factor [TGF]-beta1 and interleukin-10) were increased markedly in the gastric mucosa of H pylori-infected children compared with that of infected adults (P < .03 and < .05, respectively). Also, H pylori infection in the children was associated with markedly increased levels of gastric TGF-beta1 and interleukin-10 messenger RNA. Importantly, gastric TGF-beta1 in H pylori-infected children localized predominantly to mucosal CD25(+) and Foxp3(+) cells, indicating a Treg source for the TGF-beta1.
Conclusions:
Gastric pathology is reduced and local Treg cell responses are increased in H pylori-infected children compared with infected adults, suggesting that gastric Treg cell responses down-regulate the inflammation and ulceration induced by H pylori in children.
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