Open AccessInvestigation 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
Author(s) -
Owen Robert J,
Sharp Sally,
Lawson Andrew J,
Durrani Zarmina,
Rijpkema Sjoerd,
Kidd Mark
Publication year - 2003
Publication title -
fems immunology & medical microbiology
Language(s) - English
Resource type - Journals
eISSN - 1574-695X
pISSN - 0928-8244
DOI - 10.1016/s0928-8244(03)00022-1
Subject(s) - caga , biology , helicobacter pylori , tyrosine phosphorylation , genotype , phosphorylation , locus (genetics) , spirillaceae , tyrosine , microbiology and biotechnology , immunology , genetics , gene , gastritis , virulence , biochemistry
Isolates of Helicobacter pylori from dyspeptic patients in England and South Africa were tested for ability to induce interleukin‐8 (IL‐8) in gastric cells. All isolates were cagA ‐positive, which was used as a marker for the presence of the cag pathogenicity island. The aims were to determine if activities were related to diversity within cagE (HP0544), a locus encoding a key component in the Type IV secretion system, and if disease severity might be linked to a combination of strain features. We found that isolates were heterogeneous in ability to induce IL‐8 activity with the 23 positive isolates (59%) showing activities ranging from 260 to 3200 pg ml −1 . The cagE locus was detected in most isolates and RFLP analysis of a 1.52‐kb internal fragment showed interstrain diversity with 12 combined ( Mbo I/ Nla III) types. Most cagE genotypes were not associated with IL‐8 induction, however two genotypes were found only in IL‐8‐inducing strains and one genotype was associated with lack of IL‐8 induction. IL‐8 activity was not associated with either the number or composition of cagA tyrosine phosphorylation motifs and vacA m‐type. Although we found a weak association between cagE type and the ability to induce IL‐8, our results imply that gastric cell factors or bacterial factors other than vacA , cagA and cagE are involved in the induction of IL‐8 and the development of severe gastric disease.