Gene-expression profiles in gastric epithelial cells stimulated with spiral and coccoid Helicobacter pylori.
Human gastric epithelial immortalized GES-1 cells were infected with spiral and coccoid Helicobacter pylori. Scanning electron microscopy was used to determine the ability of the two forms of H. pylori to adhere to GES-1 cells. GES-1 cell apoptosis induced by coccoid and spiral H. pylori was analysed using flow cytometry. A cDNA microarray for 22,000 human genes was used to identify the gene-expression differences in GES-1 cells infected with the two forms of H. pylori, and the gene expression identified by the cDNA microarray was confirmed by RT-PCR. Scanning electron microscope observation showed that both coccoid and spiral bacteria can adhere to GES-1 cells. After 4 h infection, apoptosis induction was 27.4% for spiral-form infection and 10.2% for coccoid-form infection. Of 268 differentially expressed genes identified by cDNA microarray, 166 showed higher expression with the spiral H. pylori infection than with the coccoid H. pylori infection. To the best of the authors' knowledge, this is the first report that GES-1 cells infected with spiral H. pylori have higher expression of cxcl10, ccl11, ccl5, groalpha, TLR5, ATF3, fos, fosl2, gadd45a and myc. The cells infected with coccoid H. pylori had higher expression of survivin. The global profile of gene expression in GES-1 cells infected with coccoid and spiral H. pylori is described for the first time.
Liu
Zhi-Fang
ZF
The Key Laboratory of Experimental Teratology, Ministry of Education, Shandong University, 44 WenhuaXi Road, Jinan, China.
Chen
Chun-Yan
CY
Department of Oncology, the Second Hospital of Shandong University, 247 Beiyuan Road, Jinan, China.
Tang
Wei
W
Zhang
Jian-Ye
JY
Gong
Yao-Qin
YQ
The Key Laboratory of Experimental Teratology, Ministry of Education, Shandong University, 44 WenhuaXi Road, Jinan, China.
Jia
Ji-Hui
JH
The Key Laboratory of Experimental Teratology, Ministry of Education, Shandong University, 44 WenhuaXi Road, Jinan, China.
D051700:Activating Transcription Factor 3 / Q000235:genetics / Q000378:metabolism; D017209:Apoptosis; D018797:Cell Cycle Proteins / Q000235:genetics / Q000378:metabolism; D002460:Cell Line; D054413:Chemokine CCL11; D018946:Chemokine CCL5; D054357:Chemokine CXCL10; D018925:Chemokines / Q000235:genetics / Q000378:metabolism; D019742:Chemokines, CC / Q000235:genetics / Q000378:metabolism; D019743:Chemokines, CXC / Q000235:genetics / Q000378:metabolism; D004847:Epithelial Cells / Q000378:metabolism* / Q000473:pathology; D051921:Fos-Related Antigen-2 / Q000235:genetics / Q000378:metabolism; D020869:Gene Expression Profiling; D016762:Genes, fos / Q000235:genetics; D016481:Helicobacter Infections / Q000378:metabolism* / Q000382:microbiology; D016480:Helicobacter pylori / Q000648:ultrastructure; D006801:Humans; D051034:Inhibitor of Apoptosis Proteins; D008869:Microtubule-Associated Proteins / Q000235:genetics / Q000378:metabolism; D009363:Neoplasm Proteins / Q000235:genetics / Q000378:metabolism; D009687:Nuclear Proteins / Q000235:genetics / Q000378:metabolism; D016271:Proto-Oncogene Proteins c-myc / Q000235:genetics / Q000378:metabolism; D013045:Species Specificity; D013270:Stomach; D000077022:Survivin; D051198:Toll-Like Receptor 5 / Q000235:genetics / Q000378:metabolism; D000097642:GADD45 Proteins
D051700:Activating Transcription Factor 3; D018797:Cell Cycle Proteins; D054413:Chemokine CCL11; D018946:Chemokine CCL5; D054357:Chemokine CXCL10; D018925:Chemokines; D019742:Chemokines, CC; D019743:Chemokines, CXC; D051921:Fos-Related Antigen-2; D051034:Inhibitor of Apoptosis Proteins; D008869:Microtubule-Associated Proteins; D009363:Neoplasm Proteins; D009687:Nuclear Proteins; D016271:Proto-Oncogene Proteins c-myc; D000077022:Survivin; D051198:Toll-Like Receptor 5; C490449:ATF3 protein, human; C107489:BIRC5 protein, human; C515456:CCL11 protein, human; C483024:CCL5 protein, human; C497872:FOSL2 protein, human; C439070:GADD45A protein, human; D000097642:GADD45 Proteins; C489427:MYC protein, human; C495346:TLR5 protein, human