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In Situ Expression of cagA and Risk of Gastroduodenal Disease in Helicobacter pylori–infected Children

Rick, James R*; Goldman, Matthew*; Semino-Mora, Cristina; Liu, Hui; Olsen, Cara; Rueda-Pedraza, Eugenia§; Sullivan, Carolyn||; Dubois, Andre

Journal of Pediatric Gastroenterology & Nutrition: February 2010 - Volume 50 - Issue 2 - p 167–172
doi: 10.1097/MPG.0b013e3181bab326
Original Articles: Gastroenterology

Background and Aim: 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.

Patients and 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.

*Departments of Pediatrics, USA

Medicine, USA

Preventive Medicine and Biometrics, Uniformed Services University of the Health Sciences, Bethesda, MD, USA

§Departments of Pathology, USA

||Pediatrics, Walter Reed Army Medical Center, Washington, DC, USA.

Received 5 March, 2009

Accepted 30 July, 2009

Address correspondence and reprint requests to Andre Dubois, MD, PhD, USUHS, 4301 Jones Bridge Rd, Bethesda, MD 20814-4799 (e-mail: adubois@usuhs.edu).

The authors report no conflicts of interest.

J.R.R. and M.G. designed and performed the study, analyzed the data, and wrote and revised the manuscript; C.S.M. mentored J.R.R. and M.G., supervised performance and analysis of in situ hybridization studies, and revised the manuscript; H.L. designed and validated the probes used for in situ hybridization studies, and revised the manuscript; C.O. performed the statistical analysis and revised the manuscript; E.R.P. reviewed and graded histopathology sections and revised the manuscript; C.S. helped in the analysis of the clinical data and revised the manuscript; and A.D. closely supervised and participated in the design and performance of all of the steps of the study, and wrote and revised the manuscript.

The comments and opinions stated in this article are solely those of the authors and in no way reflect those of the Department of Defense, US government, US Army, or the US Air Force. The protocol was approved by the institutional review boards of Walter Reed Army Medical Center and the Uniformed Services University of the Health Sciences. Supported in part by the National Institutes of Health (CA82312) and USUHS (CO86EN-01).

© 2010 Lippincott Williams & Wilkins, Inc.