title: In situ expression of cagA and risk of gastroduodenal disease in Helicobacter pylori-infected children.
abstract: OBJECTIVE
  Gastroduodenal disease is more common among adults and children with cagA+ Helicobacter pylori infection, but disease severity varies among those infected with cagA+ strains. We examined whether cagA in situ expression can predict disease manifestations among H pylori-infected children.
  
  
  METHODS
  Fifty-one children were selected from 805 patients with abdominal symptoms who underwent esophagogastroduodenoscopy with gastric biopsies. Endoscopic and histologic gastritis were scored and H pylori colonization was quantified by Genta stain and in situ hybridization expression of 16S rRNA and cagA.
  
  
  RESULTS
  Endoscopy was either normal (n = 14) or demonstrated nodularity (n = 18), gastric ulcer (n = 8) or duodenal ulcer (n = 11). H pylori was present in 7, 18, 6, and 10 children, respectively. Expression of 16S rRNA and cagA were significantly higher in children with ulcer compared with normal children. The fraction of H pylori bacteria expressing cagA in situ was higher in children with ulcer compared to those with endoscopic nodularity (P < 0.05).
  
  
  CONCLUSIONS
  Thus, cagA in situ expression is increased in H pylori-infected children with peptic ulcers and may play a role in the pathogenesis of peptic ulcer disease during childhood. Determination of in situ expression of cagA complements traditional isolation and in vitro testing of single-colony isolates.
authors.affiliation: Department of Pediatrics, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, MD 20814, USA.
authors.forename: James R
authors.initials: JR
authors.lastname: Rick
authors.forename: Matthew
authors.initials: M
authors.lastname: Goldman
authors.forename: Cristina
authors.initials: C
authors.lastname: Semino-Mora
authors.forename: Hui
authors.initials: H
authors.lastname: Liu
authors.forename: Cara
authors.initials: C
authors.lastname: Olsen
authors.forename: Eugenia
authors.initials: E
authors.lastname: Rueda-Pedraza
authors.forename: Carolyn
authors.initials: C
authors.lastname: Sullivan
authors.forename: Andre
authors.initials: A
authors.lastname: Dubois
mesh_terms: D000293:Adolescent; D000942:Antigens, Bacterial / Q000235:genetics / Q000378:metabolism*; D001426:Bacterial Proteins / Q000235:genetics / Q000378:metabolism*; D001706:Biopsy; D002648:Child; D002675:Child, Preschool; D015169:Colony Count, Microbial; D004381:Duodenal Ulcer / Q000209:etiology* / Q000382:microbiology; D004386:Duodenum / Q000382:microbiology / Q000473:pathology; D016145:Endoscopy, Digestive System; D005260:Female; D005756:Gastritis / Q000150:complications* / Q000382:microbiology; D015870:Gene Expression; D005798:Genes, Bacterial; D016481:Helicobacter Infections / Q000150:complications* / Q000453:epidemiology / Q000382:microbiology; D016480:Helicobacter pylori / Q000235:genetics* / Q000378:metabolism / Q000472:pathogenicity; D006801:Humans; D008297:Male; D012336:RNA, Ribosomal, 16S / Q000378:metabolism; D013270:Stomach / Q000382:microbiology / Q000473:pathology; D013276:Stomach Ulcer / Q000209:etiology* / Q000382:microbiology
chemical_list: D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D012336:RNA, Ribosomal, 16S; C080866:cagA protein, Helicobacter pylori