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The urease of Helicobacter pylori has been proposed to be one of its pathogenic factors. A kanamycin resistance determinant was inserted in a cloned urease gene, and transformation-mediated allelic exchange mutagenesis was carried out to introduce the disrupted gene into the corresponding wild-type chromosomal region of a clinical isolate of H. pylori, CPY3401. The resulting mutant, HPT73, had the null activity of urease. Nude mouse stomachs were challenged with these two isogenic strains to examine the role of urease in pathogenesis. Gastritis was found in the CPY3401-challenged stomachs, from which bacteria indistinguishable from CPY3401 were recovered. There was no gastritis in the HPT73-challenged stomachs, and we could not recover H. pylori from them. These results indicated that H. pylori urease is essential for colonizing the nude mouse stomach.

A urease-negative mutant of Helicobacter pylori constructed by allelic exchange mutagenesis lacks the ability to colonize the nude mouse stomach