Disease relevance of cagE

• Prevalence of Helicobacter pylori vacA, cagA, cagE, iceA, babA2 Genotypes and Correlation with Clinical Outcome in Turkish Patients with Dyspepsia [1].
• The wild-type and vacA mutants induced severe gastritis, whereas cagE mutants induced far milder changes [2].
• In conclusion, the knocking out of the cagE gene deprived wild-type H. pylori of the pathogenicity for gastritis and gastric ulcer, suggesting that the secretion system encoded by cag pathogenicity island genes plays an essential role [2].
• METHODS: We cocultured parental Helicobacter pylori and isogenic oipA, hopZ, or cagE gene knockout mutants with gastric cancer cells [3].
• Twelve (92%) of 13 children with duodenal ulcers were infected with cagE-positive isolates, compared with only 5 (31%) of 16 with gastritis alone (P<.01) [4].

High impact information on cagE

• A mutant lacking cagE, which encodes a structural component of the TFSS, failed to up-regulate a superset of host genes, including the cagA-dependent genes, and many of the immune response genes [5].
• Mutants of the four OMPs, as well as cagE and galE from H. pylori from the U.S. and Japan, were constructed by inserting a chloramphenicol-resistant cassette into the gene [6].
• Compared with the parental 60190 strain, the picB- mutant attenuated cell cycle progression at 6 h (P < or = 0.05), and decreased apoptosis with enhanced AGS cell viability at 24 h (P < or = 0.04) [7].
• The responses of human cell lines and mouse embryonic fibroblasts to infection with wild-type H. pylori or cagE mutant were investigated [8].
• H. pylori isogenic mutants specifically lacking picA or picB, which are responsible for cytokine production by gastric cells, were less effective in the up-regulation of cyclooxygenase-2 mRNA expression and in the stimulation of prostaglandin E2 release compared with the parental wild-type strain [9].

Chemical compound and disease context of cagE

• Investigation of the biological relevance of Helicobacter pylori cagE locus diversity, presence of CagA tyrosine phosphorylation motifs and vacuolating cytotoxin genotype on IL-8 induction in gastric epithelial cells [10].

Biological context of cagE

• Mongolian gerbils were challenged with wild-type H. pylori strain TN2, which has a functional cag pathogenicity island or isogenic mutants with disrupted cagA (DeltacagA) or cagE (DeltacagE) genes [11].
• In contrast, apoptosis was not detected following infection with cagA-negative, cagE-negative, VacA-negative clinical isolates or a Campylobacter jejuni strain [12].
• All 36 strains were found to contain cagA and cagE gene and to induce CagA phosphorylation upon infection [13].
• In coculture with isogenic cagE-negative mutant ((Delta)cagE), which encodes a type IV secretion system with other genes in the cag PAI, no significant up-regulation was found [14].
• The cagE locus was detected in most isolates and RFLP analysis of a 1.52-kb internal fragment showed interstrain diversity with 12 combined (MboI/NlaIII) types [10].

Anatomical context of cagE

• An isogenic cagE mutant of H. pylori lost about 50% of its IL-12-inducing ability, suggesting a role for the cag type IV secretion system in the stimulation of dendritic cells [15].
• In summary, cagE presence appears to be essential for H. pylori-induced apoptosis of gastric parietal cells, and this effect is dependent on the activation of NF-kappaB and production of nitric oxide [16].
• METHODS: Two gastric cancer-derived epithelial cell lines were infected with H. pylori organisms of previously defined cagE and cagA status for periods of up to 24 h [17].
• Neutrophil infiltration in gastric mucosa was significantly more severe in patients infected with cagE-positive strains than in patients infected with negative strains [18].
• The role of cagPAI on cultured cells was also investigated using isogenic mutant cagE, which carries non-functional cagPAI [19].

Associations of cagE with chemical compounds

• H. pylori isolated from gastric biopsies over a 4-year period were screened by specific PCR assays for the presence of cagA, cagD, cagE and virD4 genes in the cag PAI, and for the presence of IS605 in the PAI and elsewhere in the genome [20].
• In contrast, expression of xylE in urea or picB decreased after parallel exposure to acid pH (pH 7 > 6 > 5 > 4), regardless of the growth phase [21].

Other interactions of cagE

• Multivariate regression analysis disclosed cagE (p = .006) and vacA s1a (p = .027) genotypes to be independent predictors of DU and babA2 (p = .000) and cagE (p = .013) genotypes to be independent predictors of GC [1].
• We also found that the cagE and cagT genes were less often rearranged (18%) than the cagA gene (27%) [22].

Analytical, diagnostic and therapeutic context of cagE

• The presence of vacA alleles, cagA, cagE, iceA, and babA2 genotypes were determined by polymerase chain reaction (PCR) [1].
• We examined the role of two genes, vacA and cagE, in the gastric pathogenesis induced by H. pylori using a long-term (62 wk) animal model [2].
• We compared the effects of coculture with four H pylori strains, a cag pathogenicity island (PAI) positive strain TN2, its isogenic vacA negative (TN2-DeltavacA) or cagE negative (TN2-DeltacagE) mutants, and a cag PAI negative clinical isolate T68 [23].
• As assessed by both transmission electron microscopy and fluorescence microscopy, incubation with a cagA-positive, cagE-positive, VacA-positive clinical H. pylori isolate stimulated an increase in apoptosis compared to the apoptosis of untreated AGS cells (16.0% +/- 2.8% versus 5.9% +/- 1. 4%, P < 0.05) after 72 h [12].
• Accuracy of ELISA to predict bacterial possession of cagA was 61.7% whereas 58.3% for cagE and VirD4 [24].

References