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Genetic Diversity of Helicobacter pylori Isolates in Sudan

von Dr. Wael Faroug Elamin

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[1.] Wfe/Fragment 005 01 - Diskussion
Zuletzt bearbeitet: 2015-11-29 16:47:44 Hindemith
Fragment, Gesichtet, KomplettPlagiat, SMWFragment, Schutzlevel sysop, Wanken 2003, Wfe

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[This layer of gastric mucus, about 0.2-0.6 mm thick, is secreted] by epithelial cells and plays an important protective role in the stomach, both as a lubricant and as part of the gastric mucosal barrier against acid and pepsin. H. pylori thrives in this mucus environment. The mucus layer forms a stable, continuous layer over the mucosa and provides an environment for the neutralization of luminal acid, maintaining a near neutral pH at the mucosal surface (Ferrero, 2005).

According to studies employing light and electron microscopy and examination of stained gastric biopsies, H. pylori can be found both in the gastric mucus and in close proximity to the mucosal epithelial cells where it is protected from the acidic environment of the stomach lumen (Hazell et al., 1986; Liu et al., 2006).


Ferrero, R. L., Innate immune recognition of the extracellular mucosal pathogen, Helicobacter pylori, Mol Immunol, 42, 879-885, 2005.

Hazell, S. L., A. Lee, L. Brady, and W. Hennessy, Campylobacter pyloridis and gastritis: association with intercellular spaces and adaptation to an environment of mucus as important factors in colonization of the gastric epithelium, J Infect Dis, 153, 658-663, 1986.

Liu, Y., E. Hidaka, Y. Kaneko, T. Akamatsu, and H. Ota, Ultrastructure of Helicobacter pylori in human gastric mucosa and H. pylori-infected human gastric mucosa using transmission electron microscopy and the high-pressure freezing-freeze substitution technique, J Gastroenterol, 41, 569-574, 2006.

[Page 6]

This layer of gastric mucus, about 0.2-0.6 mm thick, is secreted by epithelial cells and plays an important protective role in the stomach, both as a lubricant and as part of the gastric mucosal barrier against acid and pepsin (62).

H. pylori thrives in a mucus environment.

[Page 7]

The mucus layer forms a stable, continuous layer over the mucosa and provides an environment for the neutralization of lumenal acid, maintaining a near neutral pH at the mucosal surface (5).

According to studies employing light and electron microscopy and examination of stained gastric biopsies, H. pylori can be found both in the gastric mucus and in close proximity to the mucosal epithelial cells where it is protected from the acidic environment of the stomach lumen (17, 68).


5. Allen, A. 1984. The structure and function of gastrointestinal mucous, p. 3-11. In E. C. Boedeker (ed.), Attachment of organisms to the gut mucosa, vol. II. CRC Press, Boca Raton.

17. Boren, T., S. Normark, and P. Faulk. 1994. Helicobacter pylori: Molecular basis for host recognition and bacterial adherence. Trends in Microbiology 2:221-8.

62. Goggin, P., and T. Northfield. 1993. Mucosal defence, p. 40-. In T. C. Northfield, M. Mendall, and P. M. Goggin (ed.), Helicobacter pylori infection. Kluwer Academic Publishers, Boston.

68. Hazell, S. L., A. Lee, L. Brady, and W. Hennessy. 1986. Campylobacter pyloridis and gastritis: Association with intracellular spaces and adaptation to an environment of mucus as important factors in colonization of the gastric epithelium. The Journal of Infectious Diseases 153:658-663.

Anmerkungen

Nothing has been marked as a citation; the source is not given.

Sichter
(Graf Isolan), Hindemith

[2.] Wfe/Fragment 005 20 - Diskussion
Zuletzt bearbeitet: 2016-01-09 22:04:29 Hindemith
Fragment, Gesichtet, KomplettPlagiat, SMWFragment, Schutzlevel sysop, Wanken 2003, Wfe

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In addition to point mutations that are unique to individual strains, large gene clusters are present in some strains but not in others (Gressmann et al., 2005). Early studies revealed that about 60% of H. pylori isolates produce an immunodominant 120-140 kDa protein of unknown function (CagA) (Cover et al., 1990; Crabtree et al., 1991). The cagA gene is located within an approximately 40 kb DNA segment called the cag pathogenicity island (PAI) (Akopyants et al., 1998; Censini et al., 1996). Many of the genes within the cag PAI help H. pylori activate proinflammatory signal transduction pathways in gastric epithelial cells (Segal et al., 1996, 1997), contributing to the host inflammatory response. Infection with strains that contain the cag PAI is more likely to result in clinical disease than is colonization with cag-negative strains (Covacci et al., 1993; Cover et al., [1990; Crabtree et al., 1991).]

Akopvants, N. S,, S. W, Clifton, D. Kersulvte, J. E. Crabtree, B. E. Youree, C. A. Reece, N. O. Bukanov, E. S. Drazek, B. A. Roe, and D. E. Berg, Analyses of the eag pathogenicity island of Helicobacter pylori, Mol Microbiol, 28, 37-53, 1998.

Censini, S,, C, Lange, Z, Xiang, J, E, Crabtree, P, Ghiara, M, Borodovskv, R, Rap- puoli, and A, Covaeei, cag, a pathogenicity island of Helicobacter pylori, encodes type I-speeihe and disease-associated virulence factors, Proc Natl Acad Sci U S A, 93, 14,648-14,653, 1996.

Covacci, A,, S, Censini, M, Bugnoli, E, Petracca, D, Burroni, G, Macchia, A, Mas- sone, E, Papini, Z, Xiang, and N, Figura, Molecular characterization of the 128- kda immunodominant antigen of Helicobacter pylori associated with cytotoxicity and duodenal ulcer, Proc Natl Acad Sci U S A, 90, 5791-5795, 1993,

Cover, T, L,, C, P, Dooley, and M, J, Blaser, Characterization of and human serologic response to proteins in Helicobacter pylori broth culture supernatants with vacuolizing cytotoxin activity, Infect Immun, 58, 603-610, 1990,

Crabtree, J, E,, J, D, Taylor, J, I, Wyatt, E, V, Heatlev, T, M, Shalleross, D, S, Tompkins, and B, J, Eathbone, Mucosal iga recognition of Helicobacter pylori 120 kda protein, peptic ulceration, and gastric pathology, Lancet, 338, 332-335, 1991,

Gressmann, H,, B, Linz, R, Ghai, K, P, Pleissner, R, Sehlapbaeh, Y, Yamaoka, C. Kraft, S. Suerbaum, T, F, Meyer, and M, Aehtman, Gain and loss of multiple genes during the evolution of Helicobacter pylori, PLoS Genet, 1, 2005.

Segal, E. D,, S. Falkow, and L. S. Tompkins, Helicobacter pylori attachment to gastric cells induces evtoskeletal rearrangements and tyrosine phosphorylation of host cell proteins, Proc Natl Acad Sci U S A, 93, 1259-1264, 1996.

Segal, E. D,, C. Lange, A. Covaeei, L. S. Tompkins, and S. Falkow, Induction of host signal transduction pathways by Helicobacter pylori, Proc Natl Acad Sci U S A, 94, 7595-7599, 1997.

In addition to point mutations that are unique to individual strains, large gene clusters are present in some strains but not in others. Early studies revealed that about 60% of H. pylori isolates produce an immunodominant 120-140 kDa protein of unknown function (CagA) (35, 36). The cagA gene is located within an approximately 40 kb DNA segment called the cag pathogenicity island (PAI) (2, 23). Many of the genes within the cag PAI help H. pylori activate proinflammatory signal transduction pathways in gastric epithelial cells (145, 146), contributing to the host inflammatory response. Infection with strains that contain the cag PAI is more likely to result in clinical disease than is colonization with cag-negative strains (33, 35, 36). Therefore, the presence or absence of the cag PAI is an important characteristic among H. pylori strains.

2. Akopyants, N. S., S. W. Clifton, D. Kersulyte, J. E. Crabtree, B. E. Youree, C. A. Reece, N. O. Bukanov, E. S. Drazek, B. A. Roe, and D. E. Berg. 1998. Analyses of the cag pathogenicity island of Helicobacter pylori. Mol. Microbiol. 28:37-53.

23. Censini, S., C. Lange, Z. Xiang, J. E. Crabtree, P. Ghiara, M. Borodovsky, R. Rappuoli, and A. Covacci. 1996. cag, a pathogenicity island of Helicobacter pylori, encodes type I-specific and disease-associated virulence factors. Proc. Natl. Acad. Sci. U.S.A. 93:14648-14653.

33. Covacci, A., S. Censini, M. Bugnoli, R. Petracca, D. Burroni, G. Macchia, A. Massone, E. Papini, Z. Xiang, N. Figura, and e. al. 1993. Molecular characterization of the 128-kDa immunodominant antigen of Helicobacter pylori associated with cytotoxicity and duodenal ulcer. Proc. Natl. Acad. Sci. U.S.A. 90:5791-5795.

35. Cover, T. L., C. P. Dooley, and M. J. Blaser. 1990. Characterization of and human serologic response to proteins in Helicobacter pylori broth culture supernatants with vacuolizing cytotoxin activity. Infect. Immun. 58:603-610.

36. Crabtree, J. E., J. D. Taylor, J. I. Wyatt, R. V. Heatley, T. M. Shallcross, L. S. Tompkins, and B. J. Rathbone. 1991. Mucosal IgA recognition of Helicobacter pylori 120 kDa protein, peptic ulceration, and gastric pathology. Lancet 338:332-335.

145. Segal, E. D., S. Falkow, and L. S. Tompkins. 1995. Helicobacter pylori attachment to gastric cells induces cytoskeletal rearrangements and tyrosine phosphorylation of host cell proteins. Proc. Natl. Acad. Sci. U.S.A. 93:1259-1264.

146. Segal, E. D., C. Lange, A. Covacci, L. S. Tompkins, and S. Falkow. 1997. Induction of host signal transduction pathways by Helicobacter pylori. Proc. Natl. Acad. Sci. U.S.A. 94:7595-7599.

Anmerkungen

The source is not mentioned.

Sichter
(Hindemith) Schumann


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