Skip to main content
NCBI home page
Journal of Clinical Pathology logoLink to Journal of Clinical Pathology
. 1993 Jan;46(1):75–78. doi: 10.1136/jcp.46.1.75

Ammonium metabolism and protection from urease mediated destruction in Helicobacter pylori infection.

W D Neithercut 1, C Williams 1, M S Hossack 1, K E McColl 1
PMCID: PMC501120  PMID: 8432895

Abstract

AIM: To investigate further the intracellular ammonium metabolism of Helicobacter pylori and the mechanism of its urease mediated destruction. METHODS: The mechanism of the in vitro destruction of H pylori was investigated by incubating it in buffer solutions, at pH 6.0, containing isocitrate or alpha ketoglutarate in addition to urea concentrations which had previously been shown to destroy H pylori. RESULTS: The median (range) 5 minute survival of H pylori in 0.2 mol/l citrate buffer (pH 6.0) in the absence of urea was 88% (18-184%) and was similar to its survival in 0.2 mol/l isocitrate buffer in the absence of urea, median 88% (15-274%). In the presence of 50 mmol/l urea the survival of H pylori in the citrate buffer was reduced, 9.9% (0-146%), compared with its survival in isocitrate buffer with the same concentration of urea 37% (0-274%) (p < 0.01). A 72 hour preincubation of the organism with 10 mmol/l alpha ketoglutarate also increased the 5 minute survival of the organism in 0.2 mol/l citrate buffer containing 50 mmol/l urea to 36% (9-145%) compared with its survival in the same buffer but without preincubation with alpha ketoglutarate 0% (0-62%). CONCLUSION: The protection of H pylori from rapid destruction by the supply of compounds used in the intracellular metabolism of the ammonium shows that the urease mediated destruction of H pylori can be explained by intracellular depletion of alpha ketoglutarate as a result of over production of ammonium by uncontrolled urease activity.

Full text

PDF
75

Selected References

These references are in PubMed. This may not be the complete list of references from this article.

  1. Axon A. R. Duodenal ulcer: the villain unmasked? BMJ. 1991 Apr 20;302(6782):919–921. doi: 10.1136/bmj.302.6782.919. [DOI] [PMC free article] [PubMed] [Google Scholar]
  2. BROMBERG P. A., ROBIN E. D., FORKNER C. E., Jr The existence of ammonia in blood in vivo with observations on the significance of the NH4 plus minus NH3 system. J Clin Invest. 1960 Feb;39:332–341. doi: 10.1172/JCI104044. [DOI] [PMC free article] [PubMed] [Google Scholar]
  3. Bode G., Malfertheiner P., Nilius M., Lehnhardt G., Ditschuneit H. Ultrastructural localisation of urease in outer membrane and periplasm of Campylobacter pylori. J Clin Pathol. 1989 Jul;42(7):778–779. doi: 10.1136/jcp.42.7.778-b. [DOI] [PMC free article] [PubMed] [Google Scholar]
  4. Catrenich C. E., Makin K. M. Characterization of the morphologic conversion of Helicobacter pylori from bacillary to coccoid forms. Scand J Gastroenterol Suppl. 1991;181:58–64. [PubMed] [Google Scholar]
  5. Chittajallu R. S., Neithercut W. D., Ardill J. E., McColl K. E. Helicobacter pylori-related hypergastrinaemia is not due to elevated antral surface pH. Studies with antral alkalinisation. Scand J Gastroenterol. 1992;27(3):218–222. doi: 10.3109/00365529208999952. [DOI] [PubMed] [Google Scholar]
  6. Chittajallu R. S., Neithercut W. D., Macdonald A. M., McColl K. E. Effect of increasing Helicobacter pylori ammonia production by urea infusion on plasma gastrin concentrations. Gut. 1991 Jan;32(1):21–24. doi: 10.1136/gut.32.1.21. [DOI] [PMC free article] [PubMed] [Google Scholar]
  7. Ferrero R. L., Hazell S. L., Lee A. The urease enzymes of Campylobacter pylori and a related bacterium. J Med Microbiol. 1988 Sep;27(1):33–40. doi: 10.1099/00222615-27-1-33. [DOI] [PubMed] [Google Scholar]
  8. Greig M. A., Neithercut W. D., Hossack M., McColl K. E. Harnessing of urease activity of Helicobacter pylori to induce self-destruction of the bacterium. J Clin Pathol. 1991 Feb;44(2):157–159. doi: 10.1136/jcp.44.2.157. [DOI] [PMC free article] [PubMed] [Google Scholar]
  9. Hawtin P. R., Stacey A. R., Newell D. G. Investigation of the structure and localization of the urease of Helicobacter pylori using monoclonal antibodies. J Gen Microbiol. 1990 Oct;136(10):1995–2000. doi: 10.1099/00221287-136-10-1995. [DOI] [PubMed] [Google Scholar]
  10. Marshall B. J., Barrett L. J., Prakash C., McCallum R. W., Guerrant R. L. Urea protects Helicobacter (Campylobacter) pylori from the bactericidal effect of acid. Gastroenterology. 1990 Sep;99(3):697–702. doi: 10.1016/0016-5085(90)90957-3. [DOI] [PubMed] [Google Scholar]
  11. Marshall B. J., Goodwin C. S., Warren J. R., Murray R., Blincow E. D., Blackbourn S. J., Phillips M., Waters T. E., Sanderson C. R. Prospective double-blind trial of duodenal ulcer relapse after eradication of Campylobacter pylori. Lancet. 1988 Dec 24;2(8626-8627):1437–1442. doi: 10.1016/s0140-6736(88)90929-4. [DOI] [PubMed] [Google Scholar]
  12. Marshall B. J., McGechie D. B., Rogers P. A., Glancy R. J. Pyloric Campylobacter infection and gastroduodenal disease. Med J Aust. 1985 Apr 15;142(8):439–444. doi: 10.5694/j.1326-5377.1985.tb113444.x. [DOI] [PubMed] [Google Scholar]
  13. Megraud F., Bonnet F., Garnier M., Lamouliatte H. Characterization of "Campylobacter pyloridis" by culture, enzymatic profile, and protein content. J Clin Microbiol. 1985 Dec;22(6):1007–1010. doi: 10.1128/jcm.22.6.1007-1010.1985. [DOI] [PMC free article] [PubMed] [Google Scholar]
  14. Neithercut W. D., Greig M. A., Hossack M., McColl K. E. Suicidal destruction of Helicobacter pylori: metabolic consequence of intracellular accumulation of ammonia. J Clin Pathol. 1991 May;44(5):380–384. doi: 10.1136/jcp.44.5.380. [DOI] [PMC free article] [PubMed] [Google Scholar]
  15. Rauws E. A., Tytgat G. N. Cure of duodenal ulcer associated with eradication of Helicobacter pylori. Lancet. 1990 May 26;335(8700):1233–1235. doi: 10.1016/0140-6736(90)91301-p. [DOI] [PubMed] [Google Scholar]

Articles from Journal of Clinical Pathology are provided here courtesy of BMJ Publishing Group

RESOURCES