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

M. K R Tummuru, T. L. Cover, Martin Blaser

Research output: Contribution to journalComment/debate

126 Scopus citations

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 electrotranformation. 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.

Original languageEnglish (US)
Pages (from-to)2609-2613
Number of pages5
JournalInfection and immunity
Volume62
Issue number6
StatePublished - Jan 1 1994
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Immunology

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