Bacterial adhesion and disease activity in Helicobacter associated chronic gastritis.
PDF (1.7M)
+2 authors
Journal: 1990/April - Gut
ISSN: 0017-5749
PUBMED: 2311970
Abstract:
Ultrastructural examination of biopsies showing Helicobacter pylori associated chronic gastritis reveals close attachment between gastric surface epithelial cells and the organism. The finding of 'adhesion pedestals', which represents a cellular response to the presence of the organism, is analogous to the response of intestinal cells to enteropathogenic E coli. Thus the development of bacterial attachment sites in H pylori associated gastritis might be an indication of pathogenicity. We have therefore explored the relationship between the proportion of organisms forming attachment sites and histological indices of disease 'activity'. Antral biopsies from 40 patients with H pylori positive gastritis were examined histologically and ultrastructurally, and the percentage of attached organisms compared with subjective assessments of epithelial degeneration, mucin depletion, polymorphonuclear and chronic inflammatory cell infiltration. We found a significant increase in the proportion of attached bacteria in cases showing histological epithelial degeneration, and a significant decrease in cases showing intraepithelial polymorph infiltration. The direct relationship between bacterial attachment and cellular degeneration lends further support to a pathogenic effect. Reduced attachment in the face of polymorph infiltration might indirectly reflect aspects of the immune response--namely, blocking of adhesion by IgA, with complement activation and generation of leucotactic factors.
Open in
PUBMED | PMC | Google Scholar | Wikipedia
Relations:
Content
Citations
(88)
References
(23)
Diseases
(2)
Conditions
(1)
Organisms
(2)
Processes
(1)
Anatomy
(1)
Affiliates
(1)
Similar articles
Articles by the same authors
Discussion board
Gut 31(2): 134-138
PMID: 2311970

Bacterial adhesion and disease activity in Helicobacter associated chronic gastritis.

Abstract

Ultrastructural examination of biopsies showing Helicobacter pylori associated chronic gastritis reveals close attachment between gastric surface epithelial cells and the organism. The finding of 'adhesion pedestals', which represents a cellular response to the presence of the organism, is analogous to the response of intestinal cells to enteropathogenic E coli. Thus the development of bacterial attachment sites in H pylori associated gastritis might be an indication of pathogenicity. We have therefore explored the relationship between the proportion of organisms forming attachment sites and histological indices of disease 'activity'. Antral biopsies from 40 patients with H pylori positive gastritis were examined histologically and ultrastructurally, and the percentage of attached organisms compared with subjective assessments of epithelial degeneration, mucin depletion, polymorphonuclear and chronic inflammatory cell infiltration. We found a significant increase in the proportion of attached bacteria in cases showing histological epithelial degeneration, and a significant decrease in cases showing intraepithelial polymorph infiltration. The direct relationship between bacterial attachment and cellular degeneration lends further support to a pathogenic effect. Reduced attachment in the face of polymorph infiltration might indirectly reflect aspects of the immune response--namely, blocking of adhesion by IgA, with complement activation and generation of leucotactic factors.

Full text

Full text is available as a scanned copy of the original print version. Get a printable copy (PDF file) of the complete article (1.7M), or click on a page image below to browse page by page. Links to PubMed are also available for Selected References.
icon of scanned page 134
134
icon of scanned page 135
135
icon of scanned page 136
136
icon of scanned page 137
137
icon of scanned page 138
138

Images in this article

Figure 1
Figure 1
on p.135
Figure 2
Figure 2
on p.135
Figure 3
Figure 3
on p.136
Figure 4
Figure 4
on p.136
Figure 6
Figure 6
on p.137
Click on the image to see a larger version.

Selected References

These references are in PubMed. This may not be the complete list of references from this article.
  • Unidentified curved bacilli on gastric epithelium in active chronic gastritis. Lancet. 1983 Jun 4;1(8336):1273–1275. [PubMed] [Google Scholar]
  • Drumm B, Sherman P, Cutz E, Karmali M. Association of Campylobacter pylori on the gastric mucosa with antral gastritis in children. N Engl J Med. 1987 Jun 18;316(25):1557–1561. [PubMed] [Google Scholar]
  • Marshall BJ, McGechie DB, Rogers PA, Glancy RJ. Pyloric Campylobacter infection and gastroduodenal disease. Med J Aust. 1985 Apr 15;142(8):439–444. [PubMed] [Google Scholar]
  • Steer HW. The gastro-duodenal epithelium in peptic ulceration. J Pathol. 1985 Aug;146(4):355–362. [PubMed] [Google Scholar]
  • Goodwin CS, Armstrong JA, Marshall BJ. Campylobacter pyloridis, gastritis, and peptic ulceration. J Clin Pathol. 1986 Apr;39(4):353–365.[PMC free article] [PubMed] [Google Scholar]
  • Chen XG, Correa P, Offerhaus J, Rodriguez E, Janney F, Hoffmann E, Fox J, Hunter F, Diavolitsis S. Ultrastructure of the gastric mucosa harboring Campylobacter-like organisms. Am J Clin Pathol. 1986 Nov;86(5):575–582. [PubMed] [Google Scholar]
  • Tricottet V, Bruneval P, Vire O, Camilleri JP, Bloch F, Bonte N, Roge J. Campylobacter-like organisms and surface epithelium abnormalities in active, chronic gastritis in humans: an ultrastructural study. Ultrastruct Pathol. 1986;10(2):113–122. [PubMed] [Google Scholar]
  • Bode G, Malfertheiner P, Ditschuneit H. Pathogenetic implications of ultrastructural findings in Campylobacter pylori related gastroduodenal disease. Scand J Gastroenterol Suppl. 1988;142:25–39. [PubMed] [Google Scholar]
  • Marshall BJ, Armstrong JA, McGechie DB, Glancy RJ. Attempt to fulfil Koch's postulates for pyloric Campylobacter. Med J Aust. 1985 Apr 15;142(8):436–439. [PubMed] [Google Scholar]
  • Morris A, Nicholson G. Ingestion of Campylobacter pyloridis causes gastritis and raised fasting gastric pH. Am J Gastroenterol. 1987 Mar;82(3):192–199. [PubMed] [Google Scholar]
  • Rauws EA, Langenberg W, Houthoff HJ, Zanen HC, Tytgat GN. Campylobacter pyloridis-associated chronic active antral gastritis. A prospective study of its prevalence and the effects of antibacterial and antiulcer treatment. Gastroenterology. 1988 Jan;94(1):33–40. [PubMed] [Google Scholar]
  • Clausen CR, Christie DL. Chronic diarrhea in infants caused by adherent enteropathogenic Escherichia coli. J Pediatr. 1982 Mar;100(3):358–361. [PubMed] [Google Scholar]
  • Gray SF, Wyatt JI, Rathbone BJ. Simplified techniques for identifying Campylobacter pyloridis. J Clin Pathol. 1986 Nov;39(11):1279–1279.[PMC free article] [PubMed] [Google Scholar]
  • Luft JH. Ruthenium red and violet. I. Chemistry, purification, methods of use for electron microscopy and mechanism of action. Anat Rec. 1971 Nov;171(3):347–368. [PubMed] [Google Scholar]
  • Rothbaum R, McAdams AJ, Giannella R, Partin JC. A clinicopathologic study of enterocyte-adherent Escherichia coli: a cause of protracted diarrhea in infants. Gastroenterology. 1982 Aug;83(2):441–454. [PubMed] [Google Scholar]
  • Rosenstein IJ, Stoll MS, Mizuochi T, Childs RA, Hounsell EF, Feizi T. New type of adhesive specificity revealed by oligosaccharide probes in Escherichia coli from patients with urinary tract infection. Lancet. 1988 Dec 10;2(8624):1327–1330. [PubMed] [Google Scholar]
  • Evans DG, Evans DJ, Jr, Moulds JJ, Graham DY. N-acetylneuraminyllactose-binding fibrillar hemagglutinin of Campylobacter pylori: a putative colonization factor antigen. Infect Immun. 1988 Nov;56(11):2896–2906.[PMC free article] [PubMed] [Google Scholar]
  • Cantey JR, Blake RK. Diarrhea due to Escherichia coli in the rabbit: a novel mechanism. J Infect Dis. 1977 Mar;135(3):454–462. [PubMed] [Google Scholar]
  • Figura N, Guglielmetti P, Rossolini A, Barberi A, Cusi G, Musmanno RA, Russi M, Quaranta S. Cytotoxin production by Campylobacter pylori strains isolated from patients with peptic ulcers and from patients with chronic gastritis only. J Clin Microbiol. 1989 Jan;27(1):225–226.[PMC free article] [PubMed] [Google Scholar]
  • Nevalainen TJ, Järvi OH. Intracellular cysts in gastric carcinoma. Acta Pathol Microbiol Scand A. 1976 Nov;84(6):517–522. [PubMed] [Google Scholar]
  • Kovacs JA, Gill V, Swan JC, Ognibene F, Shelhamer J, Parrillo JE, Masur H. Prospective evaluation of a monoclonal antibody in diagnosis of Pneumocystis carinii pneumonia. Lancet. 1986 Jul 5;2(8497):1–3. [PubMed] [Google Scholar]
  • Dixon MF, Wyatt JI, Burke DA, Rathbone BJ. Lymphocytic gastritis--relationship to Campylobacter pylori infection. J Pathol. 1988 Feb;154(2):125–132. [PubMed] [Google Scholar]
  • Das SS, Karim QN, Easmon CS. Opsonophagocytosis of Campylobacter pylori. J Med Microbiol. 1988 Oct;27(2):125–130. [PubMed] [Google Scholar]
Department of Pathology, University of Leeds.
Department of Pathology, University of Leeds.
Copyright notice
Abstract
Ultrastructural examination of biopsies showing Helicobacter pylori associated chronic gastritis reveals close attachment between gastric surface epithelial cells and the organism. The finding of 'adhesion pedestals', which represents a cellular response to the presence of the organism, is analogous to the response of intestinal cells to enteropathogenic E coli. Thus the development of bacterial attachment sites in H pylori associated gastritis might be an indication of pathogenicity. We have therefore explored the relationship between the proportion of organisms forming attachment sites and histological indices of disease 'activity'. Antral biopsies from 40 patients with H pylori positive gastritis were examined histologically and ultrastructurally, and the percentage of attached organisms compared with subjective assessments of epithelial degeneration, mucin depletion, polymorphonuclear and chronic inflammatory cell infiltration. We found a significant increase in the proportion of attached bacteria in cases showing histological epithelial degeneration, and a significant decrease in cases showing intraepithelial polymorph infiltration. The direct relationship between bacterial attachment and cellular degeneration lends further support to a pathogenic effect. Reduced attachment in the face of polymorph infiltration might indirectly reflect aspects of the immune response--namely, blocking of adhesion by IgA, with complement activation and generation of leucotactic factors.
Collaboration tool especially designed for Life Science professionals.Drag-and-drop any entity to your messages.