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Microarray analysis of gastric mucosa among children with Helicobacter pylori infection
Author(s) -
Ikuse Tamaki,
Ohtsuka Yoshikazu,
Kudo Takahiro,
Hosoi Kenji,
Obayashi Naho,
Jimbo Keisuke,
Aoyagi Yo,
Fujii Tohru,
Nagata Satoru,
Shimizu Toshiaki
Publication year - 2012
Publication title -
pediatrics international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.49
H-Index - 63
eISSN - 1442-200X
pISSN - 1328-8067
DOI - 10.1111/j.1442-200x.2012.03573.x
Subject(s) - medicine , cxcl11 , helicobacter pylori , microarray analysis techniques , microarray , cxcl9 , gastritis , gastroenterology , immune system , chemokine , chronic gastritis , gastric mucosa , immunology , real time polymerase chain reaction , stomach , cxcl10 , gene expression , gene , biology , biochemistry
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.