Helicobacter pylori gastritis in children is associated with a regulatory T-cell response

PR Harris, SW Wright, C Serrano, F Riera, I Duarte… - Gastroenterology, 2008 - Elsevier
PR Harris, SW Wright, C Serrano, F Riera, I Duarte, J Torres, A Peña, A Rollán, P Viviani…
Gastroenterology, 2008Elsevier
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 …
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]-β1 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-β1 and interleukin-10 messenger RNA. Importantly, gastric TGF-β1 in H pylori–infected children localized predominantly to mucosal CD25+ and Foxp3+ cells, indicating a Treg source for the TGF-β1.
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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