There is continuing interest in identifying Helicobacter pylori virulence factors that might predict the risk for symptomatic clinical outcomes. It has been proposed thaticeA and cagA genes are such markers and can identify patients with peptic ulcers. We compared H. pylori isolates from four countries, looking at thecagA and vacA genotypes, iceAalleles, and presentation of the infection. We used PCR to examineiceA, vacA, and cagA status of 424H. pylori isolates obtained from patients with different clinical presentations (peptic ulcer, gastric cancer, and atrophic gastritis). The H. pylori isolates examined included 107 strains from Bogota, Colombia, 70 from Houston, Tex., 135 from Seoul, Korea, and 112 from Kyoto, Japan. The predominant genotype differed among countries: the cagA-positive iceA1 vacA s1c-m1 genotype was predominant in Japan and Korea, thecagA-positive iceA2 vacA s1b-m1 genotype was predominant in the United States, and the cagA-positiveiceA2 vacA s1a-m1 genotype was predominant in Colombia. There was no association between the iceA,vacA, or cagA status and clinical outcome in patients in the countries studied. iceA status shows considerable geographic differences, and neither iceA nor combinations of iceA, vacA, andcagA were helpful in predicting the clinical presentation of an H. pylori infection.

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Background-Helicobacter pylori strains possessing the cagA gene are thought to induce interleukin 8 (IL-8) in gastric mucosa. However, it is still unclear whether a relation exists between the cagA gene and the expression patterns of cytokines other than IL-8. Aims-To investigate the relation between the cagA gene and the production of various cytokine proteins using an enzyme linked immunosorbent assay (ELISA). Patients and methods-In 184 patients, the cagA gene was detected by polymerase chain reaction (PCR), and levels of production of IL-1 , IL-6, IL-7, IL-8, IL-10, and tumour necrosis factor (TNF-) in antral biopsy specimens were measured by ELISA. Results-Mucosal levels of IL-1 , IL-6, IL-8, and TNF-were significantly higher in H pylori positive than in H pylori negative patients. Furthermore, the mucosal levels of IL-1 and IL-8 were significantly higher in specimens infected with cagA positive strains than in those infected with cagA negative strains. In H pylori positive patients, the mucosal level of IL-8 was closely correlated with that of IL-1 (p<0.0001), and the mucosal level of IL-6 was closely correlated with that of TNF-(p<0.0001). Conclusion-These findings suggest that the ability to induce cytokines diVers among the strains; cagA + strains induce various kinds of cytokines and may cause severe inflammation, whereas cagA − strains induce IL-8 and IL-1 only weakly and may cause only mild inflammation. However, as most patients infected with the cagA + strains have gastritis, these strains may not be equivalent to ulcerogenic strains. (Gut 1997; 41: 442-451)

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