Abstract
The issues of cell regulation and turnover in the stomach are of critical importance as they impact directly on the important lesions of erosions, ulcers and cancer, the major complications of H. pylori disease. In uncomplicated H. pylori-associated gastritis and duodenitis an erosion or ulcer results from the inability of the epithelial dynamics adequately to maintain or repair the epithelium at an adequate rate. Further, a persistent long-term increase in epithelial turnover in many organs may predispose to neoplastic sequelae, and in this regard the stomach is no exception. The theory is that increased cell turnover results from increased mitotic activity, and this in turn provides greater opportunities for the production of abnormal cells from which clones may arise, and from which neoplasms may ultimately develop. Further, it is increasingly apparent that while regular cell turnover is associated with a 3–5-day turnover at the surface, and a turnover time measured in months in the pits, that there is a second method of cell degeneration that must be taken into account in epithelial dynamics, which is that of cell apoptosis. Further, the relationships between cell turnover, the inflammatory response and H. pylori itself need to be separated as far as possible. Because H. pylori infection in humans is always associated with at least some degree of chronic inflammatory infiltrate, some of these data necessarily come from animal sources.
This is a preview of subscription content, log in via an institution.
Buying options
Tax calculation will be finalised at checkout
Purchases are for personal use only
Learn about institutional subscriptionsPreview
Unable to display preview. Download preview PDF.
References
Huang LL, Cave DR, Gilbert JV, Wright A. Cloning and sequencing of the gene encoding an acid inhibitory protein in Helicobacter pylori. Gastroenterology. 1996;110:A927.
Kuipers EJ, Uyterlinde AM, Peña AS et al. Long-term sequelae of Helicobacter pylori gastritis. Lancet. 1995;345:1525–8.
Klinkenberg-Knol EC, Festen HPM, Jansen JBMJ et al. Long-term treatment with omeprazole for refractory reflux esophagitis: efficacy and safety. Ann Intern Med. 1994;121:161–7.
Havard TJ, Sarsfield P, Wotherspoon AC, Steer HW. Increased gastric epithelial cell proliferation in Helicobacter pylori associated follicular gastritis. J Clin Pathol. 1996;49:68–71.
Ladas SD, Katsogridakis J, Malamou H, Giannopoulou H, Kesse-Elia M, Raptis SA. Helicobacter pylori may induce bile reflux: link between H. pylori and bile induced injury to gastric epithelium. Gut. 1996;38:15–18.
Fan XG, Kelleher D, Fan XJ, Xia HX, Keeling PWN. Helicobacter pylori increases proliferation of gastric epithelial cells. Gut. 1996;38:19–22.
Cahill RJ, Xia H, Kilgallen C, Beattie S, Hamilton H, O’Morain C. Effect of eradication of Helicobacter pylori infection on gastric epithelial cell proliferation. Dig Dis Sci. 1995;40: 1627–31.
Cahill RJ, Kilgallen C, Beattie S, Hamilton H, O’Morain C. Gastric epithelial cell kinetics in the progression from normal mucosa to gastric carcinoma. Gut. 1996;38:177–81.
Lynch DA, Axon AT. Helicobacter pylori, gastric cancer and gastric epithelial kinetics. Eur J Gastroenterol Hepatol. 1995;7(Suppl. 1):S17–23.
Fraser AG, Sim R, Sankey EA, Dhillon AP, Pounder RE. Effect of eradication of Helicobacter pylori in gastric epithelial cell proliferation. Aliment Pharmacol Ther. 1994;8:167–73.
Brenes F, Ruiz B, Correa P et al. Helicobacter pylori causes hyperproliferation of the gastric epithelium: pre and post eradication indices of proliferating cell nuclear antigen. Am J Gastroenterol. 1993;88:1870–5.
Solcia E, Villani L, Luinetti O, Fiocca R. Proton-pump inhibitors, enterochromaffin-like cell growth, and Helicobacter pylori gastritis. Aliment Pharmacol Ther. 1993;7(Suppl. 1):29–31.
Taniguchi Y, Ido K, Kimura K et al. Morphological aspects of the cytotoxic action of Helicobacter pylori. Eur J Gastroenterol Hepatol. 1994;6(Suppl. 1):S17–21.
Chang K, Fujiwara Y, Wyle F, Tarnawski A. Helicobacter pylori toxin inhibits growth and proliferation of cultured gastric cancer cells-Kato II. J Physiol Pharmacol. 1993;44:17–22.
Matsui T, Matsukawa Y, Sakai T, Nakamura K, Aoike A, Kawai K. Effect of ammonia on cell cycle progression of human gastric cancer cells. Eur J Gastroenterol Hepatol. 1995;7(Suppl. 1): S79–81.
Crabtree JE, Farmery SM. Helicobacter pylori and gastric mucosal cytokines: evidence that CagA-positive strains are more virulent. Lab Invest. 1995;73:742–5.
Peek RM Jr, Miller GG, Tham KT et al. Heightened inflammatory response and cytokine expression in vivo to cagA+ Helicobacter pylori strains. Lab Invest. 1995;73:760–70.
Husson MO, Gottrand F, Vachee A et al. Importance in diagnosis of gastritis of detection by PCR of the cagA gene in Helicobacter pylori strains isolated from children. J Clin Microbiol. 1995;33: 3300–3.
Kuipers EJ, Pérez-Pérez GI, Meuwissen SGM, Blaser MJ. Helicobacter pylori and atrophic gastritis: importance of the cagA status. J Natl Cancer Inst. 1995;87:1777–80.
Weel JFL, Van der Hulst RWM, Gerrits Y et al. The interrelationship between cytotoxin-associated gene A, vacuolating cytotoxin, and Helicobacter pylori-related diseases. J Infect Dis. 1996; 173: 1171–5.
Ching CK, Wong BCY, Kwok E, Ong L, Covacci A, Lam SK. Prevalence of CagA-bearing Helicobacter pylori strains detected by the anti-CagA assay in patients with peptic ulcer disease and in controls. Am J Gastroenterol. 1996;91:949–53.
Tee W, Lambert JR, Dwyer B. Cytotoxin production by Helicobacter pylori from patients with upper gastrointestinal tract disease. J Clin Microbiol. 1995;33:1203–5.
Murakita H, Hirai M, Ito S, Azuma T, Kato T, Kohli Y. Vacuolating cytotoxin production by Helicobacter pylori isolates from peptic ulcer, atrophic gastritis and gastric carcinoma. Eur J Gastroenterol Hepatol. 1994;6(Suppl. 1):S29–31.
Sipponen P, Kimura K. Intestinal metaplasia, atrophie gastritis and stomach cancer: trends over time. Eur J Gastroenterol Hepatol. 1994;6(Suppl. 1):S79–83.
Sharp R, Babyatski R, Takagi H et al. Transforming growth factor alpha disrupts the normal program of cellular differentiation in the gastric mucosa of transgenic mice. Development. 1995; 121:149–61.
Tsujii M, Kawano S, Tsuji S et al. Cell kinetics of mucosal atrophy in rat stomach induced by long-term administration of ammonia. Gastroenterology. 1993;104:796–801.
Li H, Heiander HF. Hypergastrinemia increases proliferation of gastroduodenal epithelium during gastric ulcer healing in rats. Dig Dis Sci. 1996;41:40–8.
Jones NL, Yeger H, Cutz E, Sherman PM. Helicobacter pylori induces apoptosis of gastric antral epithelial cells in vivo. Gastroenterology. 1996; 110:A933.
Zhu GH, Ching CK, Lam SK, Sheng JZ, Wong TM, Ding SZ. Sialic acid dependent H. pylori lectin as an activator of calcium signal in cultured epithelial cells. Gastroenterology. 1996;110:A307.
Fukuda T, Arakawa Y, Fujiwara Y et al. Nitric oxide induces apoptosis in gastric mucosal cells. Gastroenterology. 1996; 110: A111.
Naito Y, Yoshikawa T, Yagi N et al. Cell growth inhibition and apoptosis induced by monochloramine in a gastric mucosal cell line. Gastroenterology. 1996; 110:A205.
Kato K, Sasano H, Ohara S et al. DNA damages caused by ammonia administration in rat stomach. Gastroenterology. 1996; 110: A150.
Higashide S, Gomez G, Rajaraman S, Thompson JC, Townsend CM Jr. The effects of gastrin and bombesin on apoptosis induced by fasting in the rat stomach. Gastroenterology. 1996; 110:A529.
Saegusa M, Takano Y, Okayasu I. Bcl-2 expression and its association with cell kinetics in human gastric carcinoma and intestinal metaplasia. J Cancer Res Clin Oncol. 1995;121:357–63.
Lauwers GY, Scott GV, Hendricks J. Immunohistochemical evidence of aberrant bcl-2 expression in gastric epithelial dysplasia. Cancer. 1994;73:2900–4.
Okuyama S, Yokota K, Yuki M. Cell proliferation and cell death (apoptosis) in epithelial tumors of the stomach — analysis of tumor tissues by the endoscopie mucosal resection. Jpn J Gastroenterol. 1995;92:130–9.
Uemura M, Mukai T, Okamoto S et al. Helicobacter pylori eradication inhibits the growth of intestinal type of gastric cancer in initial stage. Gastroenterology. 1996;110:A282.
O’Connor E, Buckley M, O’Morain C. Intestinal metaplasia and the gastric cancer cascade. Gastroenterology. 1996; 110: A214.
Khulusi S, Mendall MA, Badve S, Finlayson C, Northfield TC. Effect of Helicobacter pylori eradication on gastric metaplasia in the duodenum. Gut. 1995;36:193–7.
Hansson LE, Engstrand L, Nyrén O, Lindgren A. Prevalence of Helicobacter pylori infection in subtypes of gastric cancer. Gastroenterology. 1995;109:885–8.
Huang JQ, Sridhar S, Chen Y, Wilkinson J, Hunt RH. Do younger patients with Helicobacter pylori have a higher risk of gastric cancer? A meta-analysis between Hp seropositivity and gastric cancer. Gastroenterology. 1996;110:A532.
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 1996 Kluwer Academic Publishers and Axcan Pharma
About this chapter
Cite this chapter
Riddell, R.H. (1996). Cell regulation, differentiation and their sequelae in the Helicobacter pylori inflamed and eradicated stomach. In: Hunt, R.H., Tytgat, G.N.J. (eds) Helicobacter pylori. Springer, Dordrecht. https://doi.org/10.1007/978-94-009-1792-7_20
Download citation
DOI: https://doi.org/10.1007/978-94-009-1792-7_20
Publisher Name: Springer, Dordrecht
Print ISBN: 978-94-010-7299-1
Online ISBN: 978-94-009-1792-7
eBook Packages: Springer Book Archive