Bacterial pathogenic factors

Current Opinion in Gastroenterology

Volumn 12, Issue SUPPL. 1, 1996, Pages 11-15

  Figura, Natale ^a   Tabaqchali, Soad ^b,c,d  

^a UNIVERSITY OF SIENA   (Italy)

^b Department of Medical Microbiology ^*  (United Kingdom)

^c QUEEN MARY UNIVERSITY OF LONDON   (United Kingdom)

^d ST BARTHOLOMEW S HOSPITAL   (United Kingdom)

Author keywords

[No Author keywords available]

Indexed keywords

BACTERIAL TOXIN; BACTERIUM LIPOPOLYSACCHARIDE; BLOOD GROUP ANTIGEN; HEAT SHOCK PROTEIN; HEMOLYSIN; NEUTRALIZING ANTIBODY; PROTEIN A; SIALIDASE; SIGNAL PEPTIDE; UREASE;

AUTOIMMUNITY; BACTERIAL INFECTION; BACTERIUM CULTURE; BLOOD GROUP LEWIS SYSTEM; CYTOTOXICITY; ETIOLOGY; FLAGELLUM; GASTRITIS; GENE SEQUENCE; HELICOBACTER PYLORI; INFLAMMATION; NONHUMAN; PATHOGENESIS; PATHOGENICITY; PEPTIC ULCER; SHORT SURVEY; STOMACH LYMPHOMA;

EID: 0029960539     PISSN: 02671379     EISSN: None     Source Type: Journal    
DOI: 10.1097/00001574-199601001-00003     Document Type: Short Survey

References (48)

1. Xiang Z, Censini S, Bayeli PF, Telford JL, Figura N, Rappuoli R, Covacci A: Analysis of expression of cagA and vacA virulence factors in 43 strains of Helicobacter pylori reveals that the clinical isolates can be divided into two major types and that cagA is not necessary for expression of the vacuolating toxin. Infect Immun 1995, 63:94-98. A proposal to classify H. pylori isolates on the basis of the expression of CagA and VacA (type I) or of the expression of neither protein (type II).
2. Figura N: Helicobacter pylori exotoxins and gastroduodenal diseases associated with cytotoxic strain infection. Aliment Pharmacol Ther 1996, 10(suppl 1):79-96.
3. Telford JL, Ghiara P, Dell'Orco M, Comanducci M, Burroni D, Bugnoli M, Tecce MF, Censini S, Covacci A, Xiang Z et al.: Gene structure of the Helicobacter pylori cytotoxin and evidence of its key role in gastric disease. J Exp Med 1994, 179:1653-1658.
4. Atherton JC, Coa P, Peek RM Jr, Tummuru MKR, Blaser MJ, Cover TL: Mosaicism in vacuolating cytotoxin alleles of Helicobacter pylori. Association of specific vacA types with cytotoxin production and peptic ulceration. J Biol Chem 1995, 270:17771-17777. The vacA gene is also present in non-cytotoxic H. pylori strains, but encodes for a biologically silent protein; vacA of cytotoxic strains has a mosaic structure, genotype s1/m1 produced the highest levels of cytotoxic activity in vitro and was associated with peptic ulceration.
5. Leunk RD, Johnson PT, David BC, Kraft WG, Morgan DR: Cytotoxic activity in broth culture filtrates of Campylobacter pylori. J Med Microbiol 1988, 26: 93-99.
6. Atherton JC, Gonzales-Valencia G, Dubois A, Blaser MJ, Cover TL: The vacA product from rhesus monkey Helicobacter pylori is cytolethal but causes little vacuolation [Abstract]. Gut 1996, 38(suppl 1):A13.
7. Lupetti P, Heuser JE, Manetti R, Massari P, Lanzavecchia S, Bellon PL, Dallai R, Rappuoli R, Telford J: Oligomeric and subunit structure of the Helicobacter pylori vacuolating cytotoxin. J Cell Biol 1996, 133:801-807. An electron microscopy study has revealed that the native VacA is formed as oligomers with six or seven monomers. Data suggest a structure of VacA similar to AB-type toxins.
8. Manetti R, Massari P, Burroni D, De Bernard M, Marchini A, Olivieri R, Papini E, Montecucco C, Rappuoli R, Telford JL: The Helicobacter pylori cytotoxin: importance of native conformation for induction of neutralizing antibodies. Infect Immun 1995, 63:4476-4480. Only the multimeric form of the vacA protein elicits a neutralizing antibody response in rabbits.
9. Moll G, Papini E, Colonna R, Burroni D, Telford J, Rappuoli R, Montecucco C: Lipid interaction of the 37 kDa and 58 kDa fragments of the Helicobacter pylori cytotoxin. Eur J Biochem 1995, 234:947-952.
10. Papini E, Gottardi E, Satin B, De Bernard M, Telford JL, Massari P, Rappuoli R, Montecucco C: Detection of V-ATPase on the membrane of intracellular vacuoles induced by vacA of Helicobacter pylori. J Med Microbiol 1996, 44:1-6. The vacuolar ATPase proton pump is present on intracellular vacuoles induced by H. pylori.
11. +-ATPase of gastric cells. A target of Helicobacter pylori cytotoxic activity. FEBS Lett 1993, 334:158-160.
12. Melchers K, Weitzenegger T, Buhmann A, Steinhilber W, Sachs G, Schafer KP. Cloning and membrane topology of a P-type ATPase from Helicobacter pylori. J Biol Chem 1996, 271:446-457. Cloning and protein sequence analysis of H. pylori P-type ATPase demonstrated a unique protein involved in heavy metal cation-transporting ATPases, which belongs to a family of p-type ATPase containing eight transmembrane segments.
13. De Bernard M, Papini E, De Filippis V, Gottardi E, Telford J, Manetti R, Fontana A, Rappuoli R, Montecucco C: Low pH activates the vacuolating toxin of Helicobacter pylori which becomes acid and pepsin resistant. J Biol Chem 1995, 70:23937-23940. The VacA toxin can be acid-converted in vitro to a superactive form which acquires resistance to pepsin and possibly enables the toxin to increase the epithelial damage.
14. Fujiwara Y, Wyle F, Arakawa T, Kobayashi K, Tarnawski A: H.P. toxin reduces EGF binding to its receptor and proliferative response of human gastric Kato III cells to EGF stimulation. Important mechanism for H.P. interference with the ulcer healing [Abstract]. Gastroenterology 1995, 108:A97
15. Romano M, Ricci V, Zarrilli R, Ciacci C, Sommi P, Cover TL, Blaser MJ, Coffey RJ, Del Vecchio Blanco C, Ventura U: Helicobacter pylori and gastric mucosal healing: an in vitro study on the role of VacA and CagA [Abstract]. It J Gastroenterol 1995, 27(suppl 1):221.
16. Tummuru MKR, Cover TL, Blaser MJ: Mutation of the cytotoxin-associated cagA gene does not affect the vacuolating cytotoxin activity of Helicobacter pylori. Infect Immun 1994, 62:2609-2613.
17. - variant wild-type strains, were found to upregulate epithelial IL-B secretion and gene expression.
18. Crabtree JE, Xiang Z, Lindley IJD, Tompkins DS, Rappuoli R, Covacci A: Induction of interleukin-8 secretion from gastric epithelial cells by a CagA negative isogenic mutant of Helicobacter pylori. J Clin Pathol 1995, 48:967-969.
19. + strain, suggesting that cagA is not directly responsible for IL-8 production.
20. Huang J, O'Toole PW, Doig P, Trust TJ: Stimulation of interleukin-8 production in epithelial cell lines by Helicobacter pylori. Infect Immun 1995, 63:1732-1738. Surface proteins other than VacA and CagA are involved in IL-8 stimulation.
21. r 101 000 polypeptide. The picB gene is directly implicated in the induction of IL-8 expression in gastric epithelial cells in vitro.
22. + strains, but not CagA itself, elicited inflammation in the gastric mucosa of the mouse model.
23. Lange N, Censini S, Xiang Z, Borodovsky M, Rappuoli R, Covacci A: The cagl chromosomal region of Helicobacter pylori is type I-specific and encodes exporter molecules and invasion genes [Abstract]. In 8th International Workshop on Campylobacters, Helicobacters and Related Organisms 1995. Edited by Newell DG, Ketley J, Feldman RA. Weybridge: Central Veterinary Laboratory, 1995:Abt. E 2/3.
24. Clifton S, Roe B, Kersulyte D, Akopyants NS, Drazek ES, Berg DE: DNA sequence of cagll, a new multigene locus implicated in H. pylori virulence [Abstract]. Gut 1995, 37(suppl 1):A61.
25. + Helicobacter pylori strains. J Clin Microbiol 1995, 33:1496-1500. Patients with duodenal ulceration tested positive for anti-cagA antibodies significantly more often than patients with non-ulcer dyspepsia.
26. Tee W, Lambert JR, Pegorer M, Dwyer B: Cytotoxin production by Helicobacter pylori more common in peptic ulcer disease. J Clin Microbiol 1995, 33:1203-1205.
27. + H. pylori strains.
28. + H. pylori strains can be considered a risk factor for the development of gastric cancer, especially of the intestinal type affecting the distal stomach.
29. Husson M-O, Gottrand F, Vachee A, Dhaenens L, Martin de la Salle E, Turck D, Houcke M, Leclerc H: Importance in diagnosis of gastritis of detection by PCR of the cagA gene in Helicobacter pylori strains isolated from children. J Clin Microbiol 1995, 33:3300-3303. Children with haemorrhagic gastritis and severe active mucosal inflammation are more likely to be infected by H. pylori with the cagA gene.
30. - H. pylori strains.
31. Hussell T, Isaacson PG, Crabtree JE, Spencer J: Helicobacter pylori-specific tumour-infiltrating T cells provide contact dependent help for the growth of malignant B cells in low-grade gastric lymphoma of mucosa-associated lymphoid tissue. J Pathol 1996, 178:122-127. In patients with gastric MALT-type lymphomas, H. pylori organisms appear to stimulate T cells to infiltrate the lymphoma which, in turn, lead to the proliferation of malignant B cells.
32. Mobley HLT, Island MD, Hausinger RP: Molecular biology of microbial ureases. Microbiol Rev 1995, 59:451-480. A complete update on ureases produced by H. pylori and other ureolytic bacteria.
33. Karita M, Tsuda M, Nakazawa T: Essential role of urease in vitro and in vivo Helicobacter pylori colonisation study using a wild-type and isogenic urease mutant strain. J Clin Gastroenterol 1995, 21(suppl 1):S160-S163.
34. Eaton KA, Krakowka S: Avirulent, urease-deficient Helicobacter pylori colonises gastric epithelial explants ex vivo. Scand J Gastroenterol 1995, 30:434-437.
35. Dekigai H, Murakami M, Kita T: Mechanism of Helicobacter pylori associated gastric mucosa injury. Dig Dis Sci 1995, 40:1332-1339. Ammonia may induce toxic effects on gastric epithelial cells.
36. 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-S81.
37. Ito S, Kohli Y, Kato T, Murakita H, Ohotaki Y, Hirai M, Azuma T, Kuriyama M: Differences in urease activity in live Helicobacter pylori cultured from patients with gastroduodenal diseases. Eur J Gastroenterol Hepatol 1995, 7(suppl 1):S83-S88.
38. Allan E, Mullany P, Jones AC, Tabaqchali S: Identification and characterisation of the Helicobacter pylori gene encoding a homologue of ClpB heat shock protein of Escherichia coli. [Abstract] Guf 1995, 37(suppl 1):A90.
39. Schmitz A, Josenhans C, Suerbaum S: The H. pylori flagellar biosynthesis regulatory protein FIbA affects the expression of flagellar components on the transcriptional level and is probably a membrane protein [Abstract 245]. Gut 1995, 37(suppl 1):A245.
40. Drazek ES, Dubois A, Holmes RK, Kersulyte D, Akopyants NS, Berg DE, Warren RL: Cloning and characterization of hemolytic genes from Helicobacter pylori. Infect Immun 1995, 63:4345-4349. The characterization of six recombinant clones that confer haemolytic activity by E. coli on various animals red blood cells. The genes had separate chromosomal locations and conferred different haemolytic activities suggestive of specific pathogen-host tissue interactions.
41. Boren T, Falk P, Roth KA, Larson G, Normak S. Attachment of Helicobacter pylori to human gastric epithelium mediated by blood group antigens. Science 1993, 262:1892-1895.
42. Aspinall GO, Monteiro MA, Pang H, Walsh EJ, Moran AP: O Antigen chains in the lipopolysaccharide of Helicobacter pylori NCCT. 11637. Carbohydr Lett 1995, 1:151-156.
43. x in the host immune response.
44. x.
45. Negrini R, Lisato L, Zanella I, Cavazzini L, Guillini S, Villanacci V, Poiesi C, Albertini A, Ghielmi S: Helicobacter pylori infection induces antibodies cross reacting with human gastric mucosa. Gastroenterology 1991, 101:437-445.
46. Pérez-Pérez GI, Shepherd VL, Morrow JD, Blaser MJ: Activation of human THP-1 cells and rat bone marrow-derived macrophages by Helicobacter pylori lipopolysaccharide. Infect Immun 1995, 63:1183-1187.
47. Dwarakanath AD, Tsai HH, Sunderland D, Hart CA, Figura N, Crabtree JE, Rhodes JM: The production of neuraminidase and fucosidase by Helicobacter pylori: their possible relationship to pathogenicity. FEMS Immunol Med Microbiol 1995, 12:213-216. All H. pylori strains tested produced neuraminidase, with no relation to bacterial CagA expression. Neuraminidase increased in vitro the adherence of neutrophils to the endothelium.
48. r of 77000, 50000 and 48000, respectively, were isolated and might be involved in haeme-uptake from the host.