Role of Treg and Th17 Cells of the Gastric Mucosa in Children With Helicobacter pylori Gastritis

Objective: The aim of the present study was to examine the expression of FOXP3, interleukin (IL)-10, transforming growth factor (TGF)-beta 1, IL-17A, and T helper 17 (T(h)17) cells/FOXP3+ regulatory T (T-reg) cells balance in the gastric mucosa of children with Helicobacter pylori infection, in relation to the gastric histopathology. Methods: Antral mucosal biopsies were obtained from 20 children with H pylori(+) gastritis and 20 age- and sex-matched normal controls. Histopathology was assessed by the updated Sydney classification. Gene expression of FOXP3, IL-10, and TGF-beta 1 was analyzed by quantitative real-time polymerase chain reaction. Immunohistochemical staining for FOXP3+ T-reg and T(h)17 cells was performed. Results: The gene expression levels of FOXP3, TGF-beta 1, and IL-10 messenger RNA (mRNA) and the number of FOXP3+ T-reg were significantly higher in the H pylori(+) gastritis group than in the control group (P < 0.01). FOXP3 mRNA levels were correlated positively with TGF-beta 1 and IL-10 mRNA levels in the H pylori(+) gastritis group (P < 0.05). Furthermore, FOXP3 mRNA levels were correlated positively with the bacterial density, infiltration of polymorphonuclear cells, and mononuclear cells in the H pylori(+) gastritis group (P < 0.05). The number of T(h)17 cells was significantly higher in the H pylori(+) gastritis group than in the control group (P < 0.05). In addition, the number of T(h)17 cells was correlated negatively with the bacterial density and positively with the inflammatory scores of polymorphonuclear cells and mononuclear cells in the H pylori(+) gastritis group (P < 0.05). A negative correlation between the T(h)17 cells/FOXP3+ T-reg ratio and the bacterial density was demonstrated in the H pylori(+) gastritis group (P < 0.05). Conclusions: This study suggested that a T(h)17/T-reg balance toward a T-reg-biased response favors the persistence of bacteria, causing chronic active gastritis.