Analysis of whole genomic expression profiles of Helicobacter pylori related chronic atrophic gastritis with IL-1B-31CC/-511TT genotypes.
OBJECTIVE
Many studies have linked cytokine interleukin-1B gene polymorphisms to H. pylori-related gastric cancer development. The current study evaluated the characterization of whole genomic expression profiles of the premalignant condition: H. pylori-related chronic atrophic gastritis (CAG) with IL-1B-31CC/-511TT genotypes.


METHODS
IL-1B-31/-511 gene polymorphisms were determined by DNA sequences. RNA was extracted and expression profiles were performed using Agilent human whole genomic oligonucleotide microarrays (G4112F). The expression of three samples with H. pylori infection was compared to that of three samples without H. pylori infection from samples of six CAG patients, all with IL-1B-31CC/-511TT genotypes. Differentially expressed genes related to H. pylori-induced CAG with IL-1B-31CC/-511TT genotypes were screened and analyzed further by Gene Ontology (GO) and pathway. Validation of the microarray data was performed using qRT-PCR.


RESULTS
A total of 124 differentially expressed genes and 32 GO term annotations were identified between H. pylori positive and negative groups in the six CAG samples with IL-1B-31CC/-511TT genotypes. The signaling pathways identified were oxidative phosphorylation and epithelial cell signaling in H. pylori infection. Five overlapping genes were contained in identified GO terms and pathways: ATP6V0B, NDUFS5, NDUFV2, ATP6V1F and ATP6V1G1. Comparisons of qRT-PCR data and the previously reported data with the results of gene chips support the validity of our microarray data.


CONCLUSIONS
The H. pylori-related CAG with IL-1B-31CC/-511TT genotypes has shown to be the more malignant phenotype than H. pylori negative CAG with IL-1B-31CC/-511TT genotypes. Mitochondrial energy metabolism probably plays a crucial role as it is the molecular mechanism of host-bacterial interactions.
Wang
Shao Ying
SY
Institute of Digestive Disease, Tongji Hospital, Tongji University, Shanghai, China.
Shen
Xiao Ying
XY
Wu
Cai Yun
CY
Pan
Feng
F
Shen
Yuan Yuan
YY
Sheng
Hai Hui
HH
Chen
Xi Mei
XM
Gao
Heng Jun
HJ
D000368:Aged; D002908:Chronic Disease; D005260:Female; D005757:Gastritis, Atrophic / Q000235:genetics* / Q000382:microbiology; D020869:Gene Expression Profiling; D005838:Genotype; D016481:Helicobacter Infections / Q000150:complications*; D016480:Helicobacter pylori; D006801:Humans; D053583:Interleukin-1beta / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D020411:Oligonucleotide Array Sequence Analysis; D010085:Oxidative Phosphorylation; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015398:Signal Transduction
D053583:Interleukin-1beta