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Gut 1998;43(Supplement 1):S56-S60; doi:10.1136/gut.43.2008.S56
Copyright © 1998 BMJ Publishing Group Ltd & British Society of Gastroenterology.
Gut 1998;43(Suppl 1):S56-S60 ( July )

The life and death of Helicobacter pylori

D Scotta, D Weeksa, K Melchersb, G Sachsa

a UCLA and Wadsworth VA, Los Angeles, California, USA, b Byk Gulden, Konstanz

Correspondence to: Dr Sachs.

The first 150 words of the full text of this article appear below.

    Summary

The ability of Helicobacter pylori to survive in the varying acidity of the stomach is considered to be linked to its ability to maintain a tolerable pH in its periplasmic space by acid dependent activation of internal urease activity. Whereas survival of H pylori can occur between a periplasmic pH of 4.0 to 8.0, growth can only occur between a periplasmic pH of 6.0 to 8.0. When urease activity is only able to elevate periplasmic pH to between 4.0 and 6.0, the organisms will survive but not divide. In the absence of division, antibiotics such as clarithromycin and amoxycillin are ineffective. Proton pump inhibitors, by elevating gastric pH, would increase the population of dividing organisms and hence synergise with these antibiotics.

Colonisation of the normal stomach has been achieved only by Helicobacter spp., such as H pylori, H felis or H mustelae. These are Gram negative, motile, aerobic, spiral shaped organisms that dwell . . . [Full text of this article]


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  • Hofman, V., Ricci, V., Galmiche, A., Brest, P., Auberger, P., Rossi, B., Boquet, P., Hofman, P. (2000). Effect of Helicobacter pylori on Polymorphonuclear Leukocyte Migration across Polarized T84 Epithelial Cell Monolayers: Role of Vacuolating Toxin VacA and cag Pathogenicity Island. Infect. Immun. 68: 5225-5233 [Abstract] [Full Text]  

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