Helicobacter pylori Inhibits the Secretory Activity of Gastric Parietal Cells in Patients with Chronic Gastritis: An Ultrastructural Study

References

• Goodwin C S, Armstrong J A, Marshall BJ. Campylobacter pyloridis, gastritis, and peptic ulceration. J Clin Pathol 1986; 39: 353–65
   PubMed Web of Science ®Google Scholar
• Tricottct V, Bruneval P, Vire O, Camilleri J P. Campylobacter- like organisms and surface epithelinm abnormalities in active, chronic gastritis in humans: an ultrastructural study. Ultrastruct Pathol 1986; 10: 113–22
   PubMed Web of Science ®Google Scholar
• Bode G, Malfcrtheiner P, Ditschuneit H. Pathogenetic implications of ultrastructural findings in Campylobacter pylori related gastroduodenal disease. Scand J Gastroenterol 1988; 23: 25–39, Suppl 142
   Web of Science ®Google Scholar
• Blaser M J. Gastric Campylobacter-like organisms, gastritis and peptic ulcer disease. Gastroenterology 1987; 93: 371–83
   PubMed Web of Science ®Google Scholar
• Tytgat GNJ, Rolf T M, Rauws EA. Histologic and electron-microscopic observations in Campylobacter pylori gastroduo-denitis. Campylobacter pylori and gastroduodenal diseases, K Takemoto, K Kawai, T Shimoyama. Organizing Committee of Tokyo International Symposium on Campylobacter Pylori, Tokyo 1989; 1: 30–48
   Google Scholar
• Hui P K, Chan W Y, Cheung P S, Chan JKC, Ng CS. Pathologic changes of gastric mucosa colonized by Helicobacter pylori. Hum Pathol 1992; 23: 548–56
   PubMed Web of Science ®Google Scholar
• Chen X G, Correa P, Offerhaus J, Roddriguez E, Janney F, Hoffmann E, et al. Ultrastructure of the gastric mucosa harboring Campylobacter-ttke organisms. Am J Clin Pathol 1988; 86: 575–82
   Web of Science ®Google Scholar
• Taniguchi Y, Kimura K, Satoh K, Yoshida Y, Kihira K, Takimoto T, et al. Helicobacter pylori detected deep in gastric gland: an ultrastructural quantitative study. J Clin Gastroenterol 1995; 21: S169–73, Suppl l
   PubMed Web of Science ®Google Scholar
• Macgowan C C, Cover T L, Blaser MJ. Helicobacter pylori and gastric acid: biological and therapeutic implications. Gastroenterology 1996; 110: 926–38
   PubMed Web of Science ®Google Scholar
• Vargas M, Lee A, Fox J G, Cave D R. Inhibition of acid secretion from parietal cells by non-human-infecting Helicobacter species: a factor in colonization of gastric mucosa?. Infect Immun 1991; 59: 3694–9
   PubMed Web of Science ®Google Scholar
• Jablonowski H, Hengels K J, Kraemer N, Geis G, Opferkuch W, Strohmeyer G. Effects of Helicobacter pylori on histamine and carbachol stimulated acid secretion by human parietal cells. Gut 1994; 35: 755–7
   PubMed Web of Science ®Google Scholar
• Hoffman J S, King W K, Fox J G, Janik D, Cave DR. Rabbit and ferret parietal cell inhibition by Helicobacter species. Digest Dis Sci 1995; 40: 147–52
   PubMed Web of Science ®Google Scholar
• Black J A, Forte T M, Forte JG. Inhibition of HCl secretion and the effects on ultrastructure and electrical resistance in isolated piglet gastric mucosa. Gastroenterology 1981; 81: 509–19
   PubMed Web of Science ®Google Scholar
• Forte J G, Black J A, Forte T M, Mached T E, Wolosin JM. Ultrastructural changes related to functional activity in gastric oxyntic cells. Am J Physiol 1981; 241: G349–58, Gastrointest Liver Physiol 4
   PubMedGoogle Scholar
• Helander H F. Parietal cell structure during inhibition of acid secretion. Scand J Gastroenterol 1984; 19: 21–6, Suppl 101
   Web of Science ®Google Scholar
• Price A B. The Sydney System: histological division. J Gastroenterol Hepatol 1990; 6: 209–22
   Web of Science ®Google Scholar
• Smith JTL, Pounder R E, Nwokolo C U, Lanzon-Miller S, Evans D G, Graham D Y, et al. Inappropriate hypergastrinaemia in asymptomatic healthy subjects infected with Helicobacter pylori. Gut 1990; 31: 522–5
   PubMed Web of Science ®Google Scholar
• Helander H F, Sundell G W. Ultrastructure of inhibited parietal cells in the rat. Gastroenterology 1984; 87: 1064–71
   PubMed Web of Science ®Google Scholar
• Helander H F, Mattson H, Elm G, Ottoson S. Structure and function of rat parietal cells during treatment with omeprazole, SCH 28080, SCH 32651, or ranitidine. Scand J Gastroenterol 1990; 25: 799–809
   PubMed Web of Science ®Google Scholar
• Caselli M, Figura N, Trevisani L, Pazzi P, Guglielmetti P, Bovolenta M R, et al. Patterns of physical modes of contact between Campylobacter pylori and gastric epithelium: implications about the bacterial pathogenicity. Am J Gastroenterol 1989; 84: 511–3
   PubMed Web of Science ®Google Scholar
• Hessey S J, Spencer J, Wyatt J I, Sobala G, Rathbone B J, Axon ATR, et al. Bacterial adhesion and disease activity in Helicobacter associated chronic gastritis. Gut 1990; 31: 134–8
   PubMed Web of Science ®Google Scholar
• Wyle F A, Tarnawski A, Schulman D, Dabros W. Evidence for gastric mucosal cell invasion by Campylobacter pylori: an ultrastructural study. J Clin Gastroenterol 1990; 12: S92–8, Suppl 1
   Web of Science ®Google Scholar
• Morris A, Nicholson G. Ingestion of Campylobacter pyloridis causes gastritis and raised fasting gastric pH. Am J Gastroenterol 1987; 82: 192–9
   PubMed Web of Science ®Google Scholar
• Graham D Y, Alpert L C, Smith J L, Yoshimura H H. Iatrogenic Campylobacter pylori infection is a cause of epidemic achlorhydria. Am J Gastroenterol 1988; 83: 974–80
   PubMed Web of Science ®Google Scholar
• Cave D R, Vargas M V. Effect of a Campylobacter pylori protein on acid secretion by parietal cells. Lancet 1989; 2: 187–9
   PubMed Web of Science ®Google Scholar
• Beil W, Birkholz C, Wagner S, Sewing K F. Interaction of Helicobacter pylori and its fatty acids with parietal cells and gastric H+\Kf-ATPase. Gut 1994; 35: 1176–80
   PubMed Web of Science ®Google Scholar
• Noach L A, Bosma N B, Jansen J, Hoek F J, van Deventer SJH, Tytgat GNJ. Mucosal tumor necrosis factor-â, interleukin-1β, and interleukin-8 production in patients with Helicobacter pylori infection. Scand J Gastroenterol 1994; 29: 425–9
   PubMed Web of Science ®Google Scholar
• Levi S, Beardshall K, Swift I, Foulkes W, Playford R, Ghosh P, et al. Antral Helicobacter pylori, hypergastrinemia, and duodenal ulcers: effect of eradicating the organism. Br Med J 1989; 299: 1504–5
   PubMed Web of Science ®Google Scholar
• Moss S F, Calam J. Acid secretion and sensitivity to gastrin in patients with duodenal ulcer: effect of eradication of Helicobacter pylori. Gut 1993; 34: 888–92
   PubMed Web of Science ®Google Scholar
• El-Omar E, Penman I, Dorrian C A, Ardill JES, McColl KEL. Eradicating Helicobacter pylori infection lowers gastrin mediated acid secretion by two thirds in patients with duodenal ulcer. Gut 1993; 34: 1060–5
   PubMed Web of Science ®Google Scholar
• McColl KEL, Fullarton G M, Chittajalu R, El Nujumi A M, Macdonald AMI, Dahill S W, et al. Plasma gastrin, daytime intragastric pH, and nocturnal acid output before and at 1 and 7 months after eradication of Helicobacter pylori in duodenal ulcer subjects. Scand J Gastroenterol 1991; 26: 339–46
   PubMed Web of Science ®Google Scholar
• Wagner S, Gladziwa U, Haruma K, Varrentrapp M, Gebel M. Effect of Helicobacter pylori infection on 24 hour intragastric acidity in patients with gastritis and duodenal ulcer. Gut 1992; 33: 1024–8
   PubMed Web of Science ®Google Scholar
• Chittajallu R S, Howie C A, McColl KEL. Effect of Helicobacter pylori on parietal cell sensitivity to pentagastrin in duodenal ulcer subjects. Scand J Gastroenterol 1992; 27: 857–62
   PubMed Web of Science ®Google Scholar
• Morris A, Nicholson G. Experimental and accidental Campylobacter pylori infection of human. Campylobacter pylori in gastritis and peptic ulcer disease, MJ Blaser. Igaku-Shown, New York 1989; 61–72
   Google Scholar
• Yasunaga Y, Shimomura Y, Kanayama S, Yabu M, Nakanishi T, Miyazaki Y, et al. Improved fold width and increased acid secretion after eradication of the organism in Helicobacter pylori associated enlarged fold gastritis. Gut 1994; 35: 1571–4
   PubMed Web of Science ®Google Scholar