Pediatrics international : official journal of the Japan Pediatric Society · 2012
Microarray analysis of gastric mucosa among children with Helicobacter pylori infection.
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Ikuse Tamaki, Ohtsuka Yoshikazu, Kudo Takahiro, Hosoi Kenji, Obayashi Naho, Jimbo Keisuke, Aoyagi Yo, Fujii Tohru, Nagata Satoru, Shimizu Toshiaki
Аннотация
BACKGROUND: Although initial infection with Helicobacter pylori may occur before 5 years of age, the pediatric mucosal immune response against H. pylori is not clear. The aim of the present study was to evaluate immune responses in the H. pylori-infected gastric mucosa of children using microarray and real-time polymerase chain reaction (PCR) analysis of pediatric gastric samples.
METHODS: Gastric samples were obtained from 12 patients undergoing routine endoscopy of chronic abdominal complaints. Six patients (three boys, three girls) aged 10.1-14.6 years had evidence of H. pylori infection, and the remaining six (three boys, three girls) aged 10.3-15.5 years had no evidence of infection and presented no histological changes associated with gastritis. Microarray and real-time PCR analyses were performed, and the changes in gene expression-related immune response were also analyzed.
RESULTS: Using microarray analysis, the total number of significantly upregulated and downregulated genes (fold change >5, P < 0.01) was 21 in the antrum and 16 in the corpus when comparing patients with or without infection. Using real-time PCR, the expression of lipocalin-2 (Lcn2), C-C motif chemokine ligand (CCL) 18, C-X-C motif chemokine ligand (CXCL) 9 and CXCL11 was upregulated, while the expression of pepsinogen (PG) I and PGII was downregulated when comparing patients with or without infection.
CONCLUSIONS: Lcn2, CCL18, CXCL9, CXCL11, PGI and PGII play important roles in childhood H. pylori infection.
METHODS: Gastric samples were obtained from 12 patients undergoing routine endoscopy of chronic abdominal complaints. Six patients (three boys, three girls) aged 10.1-14.6 years had evidence of H. pylori infection, and the remaining six (three boys, three girls) aged 10.3-15.5 years had no evidence of infection and presented no histological changes associated with gastritis. Microarray and real-time PCR analyses were performed, and the changes in gene expression-related immune response were also analyzed.
RESULTS: Using microarray analysis, the total number of significantly upregulated and downregulated genes (fold change >5, P < 0.01) was 21 in the antrum and 16 in the corpus when comparing patients with or without infection. Using real-time PCR, the expression of lipocalin-2 (Lcn2), C-C motif chemokine ligand (CCL) 18, C-X-C motif chemokine ligand (CXCL) 9 and CXCL11 was upregulated, while the expression of pepsinogen (PG) I and PGII was downregulated when comparing patients with or without infection.
CONCLUSIONS: Lcn2, CCL18, CXCL9, CXCL11, PGI and PGII play important roles in childhood H. pylori infection.