Structure of cag pathogenicity island in Japanese Helicobacter pylori isolates

Background-cag pathogenicity island (PAI) is reported to be a major virulen ce factor of Helicobacter pylori. Aim-To characterise cagA and the cag PAI in Japanese H pylori strains. Methods-H pylori isolates from Japanese patients were evaluated for CagA by immunoblot, for cagA transcription by northern blot, and for cagA and 13 o ther cag PAT genes by Southern blot, cagA negative strains from Western cou ntries were also studied. Induction of interleukin-8 secretion from gastric epithelial cells was also investigated. Results-All Japanese strains retained cagA. Fifty nine of 63 (94%) strains had all the cag PAI genes. In the remaining four, cag PAI was partially del eted, lacking cagA transcripts and not producing CagA protein. Details of t he PAI of these strains were checked; three lacked cagB to cagQ (cagI) and continuously. cagS to cag13 (cagII), and the remaining one lacked cagB to c ag8. Western cagA negative strains completely lacked cag PAI including cagA . Nucleotide sequence analysis in one strain in which the cag PAI was parti ally deleted showed that the partial deletion contained 25 kb of cag PAI an d the cagA promoter. Interleukin-g induction was lower with the cag PAI par tial deletion strains than with the intact ones. All Japanese cag PAI delet ed strains were derived from patients with non-ulcer dyspepsia, whereas 41 of 59 (70%) CagA-producing strains were from patients with peptic ulcers or gastric cancer (p < 0.05). Conclusions-Most Japanese H pylori strains had the intact cag PAI. However, some lacked most of the cag PAI in spite of the presence of cagA. Thus the presence of the cagA gene is not an invariable marker of cag PAI related v irulence in Japanese strains.