Role of interferon-stimulated responsive element-like element in interleukin-8 promoter in Helicobacter pylori infection☆

Pattern of Transcription Factor Activation in Helicobacter pylori–Infected Mongolian Gerbils

“…Phosphorylation of JNK and IκB was induced in a time-dependent manner through 18 months, a pattern similar to the activation of NF-κB and ISRE binding. These data agree with results obtained from human gastric cells infected with H pylori, showing that JNK and IκB are involved in upstream NF-κB signaling and that p38 and IκB are upstream of ISRE 4,15,22,26 Immunoblots were used to examine mucosal samples from the 3 groups at 18 months. Levels of phosphorylated ERK were highest in the ulcer group, followed by the gastritis and the atrophy groups (see Supplementary Figure 3A online at www.gastrojournal.org).…”

“…In previous in vitro studies using human gastric cancer cell lines, we showed that both p50 and p65 were components of NF-κB binding complexes. 15,22,26 However, because the accuracy of commercially available antibodies against p50 in Mongolian gerbils is unknown, we cannot conclude that p50 was not present.…”

“…EMSA was performed using standard methods as previously described. 15 For semiquantitation, we used pooled nuclear extracts from the mixture of 3 WT H pylori-infected gastric mucosal specimens from the gastritis group at 18 months (standard sample). Density was measured by scanning, using the software Image J 1.36 software from the National Institutes of Health (http://rsbweb.nih.gov/ij/), and the density of samples was presented as a percentage of the standard sample.…”

“…Finally, infection with cagE mutants did not induce NF-κB or ISRE binding activities, which differed from results of whole gastric mucosa but agreed with previous reports using human gastric epithelial cell lines. 15 With the caveat that experiments in primary gerbil gastric mucosal epithelial cells may differ from stable gastric epithelial cell lines in many ways, NF-κB and ISRE binding activities appear to be activated in epithelial and submucosal cells. Activation of NF-κB and ISRE binding activities in epithelial cells appears to be cag PAI dependent, whereas activation in submucosal cells is cag PAI independent.…”

Gene expression profiling in human gastric mucosa infected with Helicobacter pylori

“…2,3 Moreover, both in vitro and in vivo studies have demonstrated that H. pylori affects intracellular signal transduction in host cells, thereby leading to the activation of different transcription factors and the induction of proinflammatory cytokines. 4,5 Interest has also been focused on the 'premalignant transition' potential of H. pylori. Studies in a model of H. pylori-induced gastritis in Mongolian gerbils have provided casual evidence for altered gastric epithelial cell apoptosis and proliferation in the development of gastric adenocarcinoma.…”