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Infection and Immunity, June 1994, p. 2609-2613, Vol. 62, No. 6
0019-9567/1994/$04.00+0     DOI:

research-article

Mutation of the cytotoxin-associated cagA gene does not affect the vacuolating cytotoxin activity of Helicobacter pylori.

M K Tummuru, T L Cover, and M J Blaser

Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee 37232-2605.

ABSTRACT

Helicobacter pylori now is recognized as an etiological agent in chronic superficial gastritis and peptic ulcer disease. Although only about 60% of H. pylori isolates produce an immunodominant 128-kDa antigen (CagA; cytotoxin-associated gene product), virtually all H. pylori-infected patients with duodenal ulceration develop a serologic response to the 128-kDa protein, which suggests an association of this gene with ulceration. The cloned cagA gene from H. pylori 84-183 was disrupted by insertion of a kanamycin resistance gene, and this inactivated cagA construct was introduced into H. pylori 84-183 by electrotransformation. Southern hybridization of kanamycin-resistant H. pylori transformants demonstrated that the wild-type cagA gene had been disrupted by insertion of the kanamycin cassette, and immunoblot analysis showed that the mutant strains no longer produced the 128-kDa CagA protein. Similar results were obtained when the cagA mutation was introduced by natural transformation into H. pylori 60190, a high-level toxin-producing strain. The cagA-negative H. pylori strains showed cytotoxin, urease, and phospholipase C activities, C3 binding and adherence similar to those of the isogenic wild-type strains. These findings demonstrate that the cagA gene product does not affect the vacuolating cytotoxin activity of H. pylori.

Infection and Immunity, June 1994, p. 2609-2613, Vol. 62, No. 6
0019-9567/1994/$04.00+0     DOI:




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