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Medium pH-dependent redistribution of the urease of Helicobacter pylori

Wu Hong¹, Kouichi Sano¹, Shinichi Morimatsu², David R. Scott³, David L. Weeks³, George Sachs³, Toshiyuki Goto^,1, Sharad Mohan¹, Fumiue Harada¹, Norihito Nakajima¹ and Takashi Nakano¹

¹Department of Microbiology, Osaka Medical College, 2-7 Daigaku-machi, Takatsuki-shi, Osaka 569-8686, Japan ²Department of Nursing, Kobe Tokiwa College, Ohtani-cho 2-6-2, Nagata-ku, Kobe, Hyogo 653-0838, Japan ³VA Greater Los Angeles Healthcare System and Department of Physiology and Medicine, University of California at Los Angeles, CA, USA

Correspondence Wu Hong wuhong{at}art.osaka-med.ac.jp

Received 11 September 2002 Accepted 19 November 2002

Helicobacter pylori is an aetiological agent of gastric disease. Although the role of urease in gastric colonization of H. pylori has been shown, it remains unclear as to where urease is located in this bacterial cell. The purpose of this study was to define the urease-associated apparatus in the H. pylori cytoplasm. H. pylori was incubated at both a neutral and an acidic pH in the presence or absence of urea and examined by double indirect immunoelectron microscopy. The density of gold particles for UreA was greatest in the inner portion of the wild-type H. pylori cytoplasm at neutral pH but was greatest in the outer portion at acidic pH. This difference was independent of the presence of urea and was not observed in the ureI-deletion mutant. Also, the eccentric shift of urease in acidic pH was not observed in UreI. After a 2 day incubation period at acidic pH, it was observed that the urease gold particles in H. pylori assembled and were associated with UreI gold particles. Urease immunoreactivity shifted from the inner to the outer portion of H. pylori as a result of an extracellular decrease in pH. This shift was urea-independent and UreI-dependent, suggesting an additional role of UreI in urease-dependent acid resistance. This is the first report of the intracellular transport of molecules in bacteria in response to changes in the extracellular environment.

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