title: Role of Treg and TH17 cells of the gastric mucosa in children with Helicobacter pylori gastritis.
abstract: OBJECTIVE
  The aim of the present study was to examine the expression of FOXP3, interleukin (IL)-10, transforming growth factor (TGF)-β1, IL-17A, and T helper 17 (TH17) cells/FOXP3+ regulatory T (Treg) 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-β1 was analyzed by quantitative real-time polymerase chain reaction. Immunohistochemical staining for FOXP3+ Treg and TH17 cells was performed.
  
  
  RESULTS
  The gene expression levels of FOXP3, TGF-β1, and IL-10 messenger RNA (mRNA) and the number of FOXP3+ Treg 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-β1 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 TH17 cells was significantly higher in the H pylori(+) gastritis group than in the control group (P < 0.05). In addition, the number of TH17 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 TH17 cells/FOXP3+ Treg ratio and the bacterial density was demonstrated in the H pylori(+) gastritis group (P < 0.05).
  
  
  CONCLUSIONS
  This study suggested that a TH17/Treg balance toward a Treg-biased response favors the persistence of bacteria, causing chronic active gastritis.
authors.affiliation: *Department of Pediatrics †Department of Pathology ‡Department of Biochemistry, Ewha Womans University School of Medicine, Seoul, Republic of Korea.
authors.forename: Joo Hyun
authors.initials: JH
authors.lastname: Gil
authors.forename: Jeong Wan
authors.initials: JW
authors.lastname: Seo
authors.forename: Min-Sun
authors.initials: MS
authors.lastname: Cho
authors.forename: Jung-Hyuck
authors.initials: JH
authors.lastname: Ahn
authors.forename: Hye Youn
authors.initials: HY
authors.lastname: Sung
mesh_terms: D000293:Adolescent; D016022:Case-Control Studies; D002648:Child; D002675:Child, Preschool; D005260:Female; D051858:Forkhead Transcription Factors / Q000235:genetics / Q000378:metabolism; D005753:Gastric Mucosa / Q000276:immunology* / Q000378:metabolism / Q000382:microbiology / Q000473:pathology; D005756:Gastritis / Q000276:immunology* / Q000378:metabolism / Q000382:microbiology / Q000473:pathology; D016481:Helicobacter Infections / Q000276:immunology* / Q000378:metabolism / Q000382:microbiology / Q000473:pathology; D016480:Helicobacter pylori / Q000254:growth & development*; D006801:Humans; D007249:Inflammation / Q000378:metabolism; D016753:Interleukin-10 / Q000235:genetics / Q000378:metabolism; D020381:Interleukin-17 / Q000378:metabolism; D007963:Leukocytes, Mononuclear / Q000378:metabolism; D008297:Male; D012333:RNA, Messenger / Q000378:metabolism; D050378:T-Lymphocytes, Regulatory / Q000378:metabolism*; D058504:Th17 Cells / Q000378:metabolism*; D053773:Transforming Growth Factor beta1 / Q000235:genetics / Q000378:metabolism
chemical_list: C418974:FOXP3 protein, human; D051858:Forkhead Transcription Factors; D020381:Interleukin-17; D012333:RNA, Messenger; D053773:Transforming Growth Factor beta1; D016753:Interleukin-10