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Role of bacterial amines in H. pylori-associated hypergastrinaemia

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Helicobacter pylori

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Abstract

Increasing evidence suggests that Helicobacter pylori plays an important role in the pathogenesis of duodenal ulcer disease. The bacterium is present in the gastric antrum in over 90% of individuals with duodenal ulcer1,2, and eradication of the organism decreases recurrence of duodenal ulcers significantly3,4. However, the pathogenic mechanisms whereby H. pylori infection predisposes to formation of duodenal ulcer disease are not known with certainty5. Possible mechanisms include: (1) disruption of the mucosal barrier by bacterial products such as ammonia, cytotoxin and phospholipase A2 6–8; (2) enhancement of aggressive factors such as acid, pepsin and platelet-activating factor9,10; (3) activation of monocytes and macrophages by release of cytokines such as tumour necrosis factor, interleukin 1 and reactive oxygen metabolites11; (4) immune crossreactivity between H. pylori and gastric tissue12; and (5) enhanced release of gastrin13, possibly resulting in increased production of acid and/or pepsin.

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References

  1. Marshall BJ. Campylobacter pylori: its link to gastritis and peptic ulcer disease. Rev Infect Dis. 1990;12:S87–93.

    Article  PubMed  Google Scholar 

  2. Peterson WL. Helicobacter pylori and peptic ulcer disease. N Engl J Med. 1991;324:1043–8.

    Article  PubMed  CAS  Google Scholar 

  3. Graham DY, Go MF. Helicobacter pylori: current status. Gastroenterology. 1993; 105: 279–82.

    PubMed  CAS  Google Scholar 

  4. Axon ATR. Helicobacter pylori therapy: effect on peptic ulcer disease. J Gastroenterol Hepatol. 1991;6:131–42.

    Article  PubMed  CAS  Google Scholar 

  5. Dunn BE. Pathogenic mechanisms of Helicobacter pylori. Gastroenterol Clin N Am. 1993; 22: 43–57.

    CAS  Google Scholar 

  6. Smoot DT, Mobley HLT, Chippendale GR, Lewison JF, Resau JH. Helicobacter pylori urease activity is toxic to human gastric epithelial cells. Infect Immun 1990; 58: 1992–6.

    PubMed  CAS  Google Scholar 

  7. Cover TL, Dooley CP, Blaser MJ. Characterization of and human serologic response to proteins in Helicobacter pylori broth culture supernatants with vacuolizing cytotoxin activity. Infect Immun 1990; 58: 603–10.

    PubMed  CAS  Google Scholar 

  8. Langton SR, Cesareo SD. Helicobacter pylori associated phospholipase A2 activity: a factor in peptic ulcer production? J Clin Pathol. 1992; 45: 221–4.

    Article  PubMed  CAS  Google Scholar 

  9. Dixon M. Acid, ulcers, and H. pylori. Lancet. 1993; 342: 384–5.

    Article  PubMed  CAS  Google Scholar 

  10. Denizot Y, Sobhani I, Rambaud J-C, Lewin M, Thomas Y, Benveniste J. Paf-acether synthesis by Helicobacter pylori. Gut. 1990; 31: 1242–5.

    Article  PubMed  CAS  Google Scholar 

  11. Mai UEH, Perez-Perez GI, Wahl LM, Blaser MJ, Smith PD. Soluble surface proteins from Helicobacter pylori activate monocytes/macrophages by lipopolysaccharide-independent mechanism. J Clin Invest. 1991; 87: 894–900.

    Article  PubMed  CAS  Google Scholar 

  12. Negrini R, Lisato L, Zanella I et al. Helicobacter pylori infection induces antibodies cross-reacting with human gastric mucosa. Gastroenterology. 1991; 101: 437–45.

    PubMed  CAS  Google Scholar 

  13. Levi S, Beardshall K, Playford R, Ghosh P, Haddad G, Calam J. Campylobacter pylori and duodenal ulcers: the gastrin link. Lancet. 1989; 1: 1167–8.

    Article  PubMed  CAS  Google Scholar 

  14. Graham DY, Opekun A, Lew GM, Evans DJ Jr, Klein PD, Evans DG. Ablation of exaggerated meal-stimulated gastrin release in duodenal ulcer patients after clearance of Helicobacter (Campylobacter) pylori infection. Am J Gastroenterol. 1990; 85: 394–8.

    PubMed  CAS  Google Scholar 

  15. Levi S, Beardshall K, Swift I et al. Antral Helicobacter pylori, hypergastrinaemia, and duodenal ulcers: effect of eradicating the organism. BMJ. 1989; 299: 1504–7.

    Article  PubMed  CAS  Google Scholar 

  16. Prewett EJ, Smith JTL, Nwokolo CU, Hudson M, Sawyer AM, Pounder RE. Eradication of Helicobacter pylori abolishes 24-hour hypergastrinaemia: a prospective study in healthy subjects. Aliment Pharmacol Ther. 1991; 5: 283–90.

    Article  PubMed  CAS  Google Scholar 

  17. Dial E, Tatsumi Y, Hall L, Romero J, Lichtenberger L. Synergistic interaction of gastric inflammation and luminal ammonia in gastrin release. Poster 14, Proceedings of Helicobacter pylori: basic mechanisms to clinical cure, Amelia Island, FL, 3–6 Nov. 1993.

    Google Scholar 

  18. Hunt RH. pH and Hp - Gastric acid secretion and Helicobacter pylori: implications for ulcer healing and eradication of the organism. Am J Gastroenterol. 1993;88:481–3.

    PubMed  CAS  Google Scholar 

  19. Kelly SM, Crampton J, Hunter JO. Helicobacter pylori increases the pH of the gastric mucosa in vivo. Gut. 1990; 31: A1177.

    Google Scholar 

  20. Blaser MJ. Hypotheses on the pathogenesis and natural history of Helicobacter pylori-induced inflammation. Gastroenterology. 1992; 102: 720–7.

    PubMed  CAS  Google Scholar 

  21. Chittajallu RS, Howie CA, McColl KEL. Effect of Helicobacter pylori on parietal cell sensitivity to pentagastrin in duodenal ulcer patients. Scand J Gastroenterol. 1992; 27: 857–62.

    Article  PubMed  CAS  Google Scholar 

  22. Golodner EH, Territo MC, Walsh JH, Soll AH. Stimulation of gastrin release from cultured canine G cells by Helicobacter pylori and mononuclear cells. Gastroenterology. 1992; 102: A630.

    Google Scholar 

  23. Calam J, Goodlad RA, Lee CY et al. Achlorhydria-induced hypergastrinaemia: the role of bacteria. Clin Sci. 1991; 80: 281–4.

    PubMed  CAS  Google Scholar 

  24. Moss SF, Legon S, Bishop AE, Polak JM, Calam J. Effect of Helicobacter pylori on gastric somatostatin in duodenal ulcer disease. Lancet. 1992; 340: 930–2.

    Article  PubMed  CAS  Google Scholar 

  25. Kaneko H, Nakada K, Mitsuma T et al. Helicobacter pylori infection induces a decrease in immunoreactive-somatostatin concentrations of human stomach. Dig Dis Sci. 1992; 37: 409–16.

    Article  PubMed  CAS  Google Scholar 

  26. Wu V, Sumii K, Tari A, Sumii M, Walsh JH. Regulation of rat antral gastrin and somatostatin gene expression during starvation and after refeeding. Gastroenterology. 1991; 101: 1552–8.

    PubMed  CAS  Google Scholar 

  27. Morrison RT, Boyd RN. Organic chemistry, 3rd edn. Boston: Allyn & Bacon; 1973: 727–44.

    Google Scholar 

  28. D’Amato RF, Bottone EJ, Amsterdam D. Substrate profile systems for the identification of bacteria and yeasts by rapid and automated approaches. In: Balows A, Hausler WJ Jr, Herrmann K, Isenberg HD, Shadomy HJ, editors. Manual of clinical microbiology. Washington, DC: American Society for Microbiology; 1991: 128–36.

    Google Scholar 

  29. Lichtenberger LM, Graziani LA, Dubinsky WP. Importance of dietary amines in meal-induced gastrin release. Am J Physiol. 1982; 243: 6341–7.

    Google Scholar 

  30. Lichtenberger LM, Nelson AA, Graziani LA. Amine trapping: physical explanation for the inhibitory effect of gastric acidity on the postprandial release of gastrin. Gastroenterology. 1986; 90: 1223–31.

    PubMed  CAS  Google Scholar 

  31. DelValle J, Yamada T. Amino acids and amines stimulate gastrin release from canine antral G-cells via different pathways. J Clin Invest. 1990; 85: 139–43.

    Article  PubMed  CAS  Google Scholar 

  32. Dial EJ, Cooper LC, Lichtenberger LM. Amino acid-and amine-induced gastrin release from isolated rat endocrine granules. Am J Physiol. 1991; 260: 6175–81.

    Google Scholar 

  33. Graham DY, Go MF, Evans DJ Jr. Review article: urease, gastric ammonium/ammonia, and Helicobacter pylori - the past, the present and recommendations for future research. Aliment Pharmacol Ther. 1992; 6: 659–69.

    Article  PubMed  CAS  Google Scholar 

  34. Bromberg PA, Robin ED, Forkner CE. The existence of ammonia in blood in vivo with observations of the significance of the NH4 +-NH3 system. J Clin Invest. 1960; 39: 332–41.

    Article  PubMed  CAS  Google Scholar 

  35. Graham DY, Opekune A, Lew GM, Klein PD, Walsh JH. Helicobacter pylori-associated exaggerated gastrin release in duodenal ulcer patients. The effect of bombesin infusion and urea ingestion. Gastroenterology. 1991; 100: 1571–5.

    PubMed  CAS  Google Scholar 

  36. Hazell SL, Mendz GL. The metabolism and enzymes of Helicobacter pylori: function and potential virulence factors. In: Goodwin GC, Worsley BW, editors. Helicobacter pylori: biology and clinical practice. Boca Raton: CRC Press; 1993: 115–41.

    Google Scholar 

  37. Beardshall K, Adamson D, Gill J, Unwin R, Calam J. Helicobacter pylori raises the pH of the juxta epithelial region of the mucus layer of the gastric antrum and body. Gut. 1991; 32: A569.

    Google Scholar 

  38. El Nujumi AM, Dorian CA, Chittajallu RS, Neithercut WD, McColl KE. Effect of inhibition of H. pylori urease activity by acetohydroxamic acid on serum gastrin in duodenal ulcer patients. Gut. 1991; 32: 866–9.

    Article  PubMed  Google Scholar 

  39. Chittajallu RS, Neithercut WD, Ardill JES, McColl KEL. Helicobacter pylori-related hypergastrinemia is not due to elevated antral surface pH. Scand J Gastroenterol. 1992; 27: 218–22.

    Article  PubMed  CAS  Google Scholar 

  40. Moss SF, Playford RJ, Ayesu K, Li SK, Calam J. pH-dependent secretion of gastrin in duodenal ulcer disease: effect of suppressing Helicobacter pylori. Digestion. 1992; 52: 173–8.

    Article  PubMed  CAS  Google Scholar 

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Authors
  1. B. E. Dunn
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Editors and Affiliations

  1. Division of Gastroenterology, McMaster University Medical Centre, 1200 Main Street West, Hamilton, Ontario, L8N 3Z5, Canada

    Richard H. Hunt (Professor of Medicine, Director) (Professor of Medicine, Director)

  2. Department of Gastroenterology and Hepatology, Academic Medical Centre, 9 Meibergdreef, 1105 AZ, Amsterdam, The Netherlands

    Guido N. J. Tytgat (Professor) (Professor)

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© 1994 Springer Science+Business Media Dordrecht

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Dunn, B.E. (1994). Role of bacterial amines in H. pylori-associated hypergastrinaemia. In: Hunt, R.H., Tytgat, G.N.J. (eds) Helicobacter pylori. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-1418-9_24

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  • DOI: https://doi.org/10.1007/978-94-011-1418-9_24

  • Publisher Name: Springer, Dordrecht

  • Print ISBN: 978-94-010-4620-6

  • Online ISBN: 978-94-011-1418-9

  • eBook Packages: Springer Book Archive

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