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Autor     Amy E. Wanken
Titel    Helicobacter pylori colonization of the mouse gastric mucosa: the entner-doudoroff pathway and development of a promoter-trapping system
Jahr    2003
Seiten    158
Anmerkung    Dissertation Presented in Partial Fulfillment of the Requirements for the Degree Doctor of Philosophy in the Graduate School of The Ohio State University
URL    http://rave.ohiolink.edu/etdc/view?acc_num=osu1059079727

Literaturverz.   

no
Fußnoten    no
Fragmente    9


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Chapter 1

INTRODUCTION

1.1 Helicobacter pylori

1.1.1 History

Spiral organisms in the stomachs of mammals were first reported in 1893 in Turin by Bizzozero. By the end of 1940, two additional reports of spiral gastric bacteria had appeared (Marshall, 2001). Although it was noted in 1924 by Murray Luck that the human stomach contains abundant urease activity and it was shown in 1959 that this activity disappeared after antibiotic treatment (indicating that the enzyme was of bacterial origin), the connection between gastric urease and gastric spiral bacteria was not established until the culturing of H. pylori in 1982 (Marshall and Warren, 1984). Research on gastric bacteria was at first impeded by the general belief that bacteria could not live in the acidic environment of the stomach. It was not until 1982 that H. pylori was first cultured by a research scientist, Barry Marshall, through the encouragement of a pathologist, Robin Warren. The first successful culture occurred by chance when a biopsy was left in the incubator for 5 days over the Easter holidays. By 1984, other groups had independently reported the disease associations of the organism (Langenberg et al., 1984; McNulty and Watson, 1984). Marshall hypothesized that the new bacterium was a Campylobacter found in the pyloric region of the stomach and therefore called it Campylobacter pyloridis, even though the new organism had different flagellar morphology than campylobacters.


Langenberg, M., G. Tytgat, M. Schipper, P. Rietra, and H. Zanen, Campylobacter like organisms in the stomach of patients and healthy individuals, The Lancet, 323, 1348-1349, 1984.

Marshall, B. J., One hundred years of discovery and rediscovery of Helicobacter pylori and its association with peptic ulcer disease, chap. 3, pp. 19-24, Helicobacter pylori: Physiology and genetics; ASM, 2001.

Marshall, B. J., and J. R. Warren, Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulceration, Lancet, 1, 1311-1315, 1984.

McNulty, C. A., and D. M. Watson, Spiral bacteria of the gastric antrum, Lancet, 1, 1068-1069, 1984.

[Page 1]

CHAPTER 1

INTRODUCTION

History

Spiral organisms in the stomachs of mammals were discovered more than 125 years ago in 1874, and spiral bacteria were first reported in the human stomach in 1906. By the end of 1940, two additional reports of spiral gastric bacteria had appeared (64). Although it was noted in 1924 that the human stomach contains abundant urease activity (137) and it was shown in 1959 that this activity disappeared after antibiotic treatment (indicating that the enzyme was of bacterial origin), the connection between gastric urease and gastric spiral bacteria was not established until the culturing of H. pylori in 1983 (102, 103, 165).

Research on gastric bacteria was at first impeded by the general belief that bacteria could not live in the acidic environment of the stomach (64, 137). It was not until 1983 that H. pylori was first cultured by a research scientist, Barry Marshall, through the encouragement of a pathologist, Robin Warren (102).

[Page 2]

The first successful culture occurred by chance when a biopsy was left in the incubator for 5 days over the Easter holidays in April 1982 (64, 137). By 1984, two other groups had independently reported the disease associations of the organism (137). Marshall hypothesized that the new bacterium was a Campylobacter found in the pyloric region of the stomach and therefore called it Campylobacter pyloridis (102), even though the new organism had different flagellar morphology than campylobacters.


64. Goodwin, S. 1993. Historical and microbiological perspectives, p. 1-10. In T. C. Northfield, M. Mendall, and P. M. Goggin (ed.), Helicobacter pylori infection: Pathophysiology, epidemiology, and management. Kluwer Academic Publishers, Boston.

102. Marshall, B. J., H. Royce, D. I. Annear, C. S. Goodwin, J. W. Pearman, J. R. Warren, and J. A. Armstrong. 1984. Original isolation of Campylobacter pyloridis new species from human gastric mucosa. Microbios Lett. 25:83-88.

103. Marshall, B. J., and J. R. Warren. 1984. Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulceration. Lancet 1:1311-5.

137. Rathbone, B. J., and R. V. Heatley. 1992. The historical associations between bacteria and peptic ulcer disease, p. 1-4. In B. J. Rathbone and R. V. Heatley (ed.), Helicobacter pylori and gastroduodenal disease, 2nd ed. Blackwell Scientific Publications, Oxford.

165. Warren, J. R., and B. Marshall. 1983. Unidentified curved bacilli on gastric epithelium in active chronic gastritis. The Lancet:1273-5.

Anmerkungen

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C. pyloridis became C. pylori when linguists pointed out that the former was grammatically incorrect (Marshall et al., 1987), and Campylobacter became Helicobacter when it was discovered that its 16S ribosomal RNA was clearly distinct from other Campylobacter species tested (Andersen and Wadström, 2001). In 2005, Warren and Marshall were awarded the Nobel Prize in Medicine for their work on H. pylori.

1.1.2 General characteristics

Helicobacter pylori is a gram-negative, curved or slightly spiral, microaerophilic, slow-growing organism. The most characteristic of it's [sic] enzymes is a potent multisubunit urease. H. pylori is motile and possesses five to seven sheathed polar flagella (Geis et al., 1989; Josenhans et al., 1995). The bacterium's unique feature is its ability to colonize the stomach.

Because of the relevance of this organism to human health, an effort was made to sequence the genome. H. pylori 26695, originally isolated from a gastritis patient in the United Kingdom, was the strain chosen for sequencing because it colonizes piglets and elicits immune and inflammatory responses (Tomb et al., 1997). Strain J99 was sequenced in order to permit within-species genome comparison (Alm et al., 1999). The H. pylori genomes consist of a circular chromosome approximately 1.7 Mb in size. Of the 1590 predicted coding sequences, 279 genes were H. pylori specific. Some of these species-specific genes are thought to play an important role in adaptation of H. pylori to the human stomach. The organism appears to have a limited metabolic and biosynthetic capacity. These characteristics are consistent with those of an organism that colonizes a restricted ecological niche (Tomb et al., 1997). One interesting feature of the genome is that many predicted proteins, including urease, are most closely related to corresponding proteins from gram-positive organisms, archaea, or eukaryotes, rather than from other gram-negative organisms (Tomb et al., 1997), suggesting horizontal gene transfer during the evolution of H. pylori (Garcia-Vallvé et al., 2002; Gressmann et al., 2005).


Alm, R. A., L. S. Ling, D. T. Moir, B. L. King, E. D. Brown, P. C. Doig, D. R. Smith, B. Noonan, B. C. Guild, B. L. deJonge, G. Carmel, P. J. Tummino, A. Caruso, M, Uria-Nickelsen, D. M, Mills, C. Ives, R. Gibson, D. Merberg, S. D. Mills, Q. Jiang, D. E. Taylor, G. F. Vovis, and T. J. Trust, Genomic-sequence comparison of two unrelated isolates of the human gastric pathogen Helicobacter pylori, Nature, 397, 176-180, 1999.

Andersen, L. P., and T. Wadstrom, Basic bacteriology and culture, chap, 4, pp, 27-38, Helicobacter pylori: Physiology and genetics; ASM. 2001,

Garcia-Vallve, S., P. J. Janssen, and C. A. Ouzounis, Genetic variation between Helicobacter pylori strains: gene acquisition or loss?, Trends Microbiol, 10, 445447, 2002.

Geis, G., H. Leying, S. Suerbaum, U. Mai, and W. Opferkuch, Ultrastrueture and chemical analysis of Campylobacter pylori flagella, J Clin Microbiol, 27, 436-441, 1989.

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

Josenhans, C., A. Labigne, and S. Suerbaum, Comparative ultrastruetural and functional studies of Helicobacter pylori and Helicobacter mustelae flagellin mutants: both flagellin subunits, flaA and flaB, are necessary for full motility in Helicobacter species, J Bacteriol, 177, 3010-3020, 1995.

Marshall, B. J., E. W. McCallum, and C. Prakash, Campylobacter pyloridis and gastritis, Gastroenterology, 92, 2051-2051, 1987.

Tomb, J. F., O. White, A. E. Kerlavage, E. A. Clayton, G. G. Sutton, E. D. Fleischmann, K. A. Ketchum, H. P. Klenk, S. Gill, B. A. Dougherty, K. Nelson, J. Quackenbush, L. Zhou, E. F. Kirkness, S. Peterson, B. Loftus, D. Eichardson, E. Dodson, H. G. Khalak, A. Glodek, K. McKenney, L. M. Fitzegerald, N. Lee, M. D. Adams, E. K. Hickey, D. E. Berg, J. D. Gocayne, T. E. Utterback, J. D. Peterson, J. M. Kelley, M. D. Cotton, J. M. Weidman, C. Fujii, C. Bowman, L. Watthey, E. Wallin, W. S. Hayes, M. Borodovsky, P. D. Karp, H. O. Smith, C. M. Fraser, and J. C. Venter, The complete genome sequence of the gastric pathogen Helicobacter pylori, Nature, 388, 539-547, 1997.

C. pyloridis became C. pylori when linguists pointed out that the former was grammatically incorrect (101), and Campylobacter became Helicobacter when it was discovered that its 16S ribosomal RNA was clearly distinct from other Campylobacter species tested (63).

General characteristics

Helicobacter pylori is a gram-negative, curved or slightly spiral, microaerophilic, slow-growing organism. Its most characteristic enzyme is a potent multi-subunit urease. H. pylori is motile and possesses four to six sheathed polar flagella (80, 150). The bacterium’s unique feature is its ability to colonize the stomach. [...]

Because of the relevance of this organism to human health, an effort was made to sequence the genome. H. pylori 26695, originally isolated from a gastritis patient in

[page 3]

the United Kingdom, was the strain chosen for sequencing because it colonizes piglets and elicits immune and inflammatory responses (157). Strain J99 was later sequenced (7). The H. pylori genomes consist of a circular chromosome approximately 1.7 Mb in size. Of the 1590 predicted coding sequences, 594 lack homology to E. coli or H. influenzae genes (76). 499 of these lacked obvious homology to any sequences in databases at the time of annotation, in 1997 (34). Some of these species-specific genes no doubt play an important role in adaptation of H. pylori to the human stomach.

[...] The organism appears to have a limited metabolic and biosynthetic capacity. These characteristics are consistent with those of an organism that colonizes a restricted ecological niche (157). One interesting feature of the genome is that many predicted proteins, including urease, are most closely related to corresponding proteins from Gram-positive organisms, Archaea, or eukaryotes, rather than from other Gram-negative organisms (157), suggesting horizontal gene transfer during the evolution of H. pylori.


7. Alm, R., L.-S. L. Ling, D. T. Moir, B. L. King, E. D. Brown, P. C. Doig, D. R. Smith, B. Noonan, B. C. Guild, B. L. deJonge, G. Carmel, P. J. Tummino, A. Caruso, M. Uria-Nickelsen, D. M. Mills, C. Ives, R. Gibson, D. Merberg, S. D. Mills, Q. Jiang, D. E. Taylor, G. F. Vovis, and T. J. Trust. 1999. Genomic-sequence comparison of two unrelated isolates of the human gastric pathogen Helicobacter pylori. Nature 397:176-180.

34. Cover, T. L., D. E. Berg, M. J. Blaser, and H. L. T. Mobley. 2001. H. pylori pathogenesis, p. 509-558. In E. A. Groisman (ed.), Principles of Bacterial Pathogenesis. Academic Press, San Diego.

63. Goodwin, C. S. 1994. How Helicobacter pylori acquired its name, and how it overcomes gastric defence mechanisms. Journal of Gastroenterology and Hepatology 9:S1-3.

76. Huynen, M., T. Dandelkar, and P. Bork. 1998. Differential genome analysis applied to the species-specific features of Helicobacter pylori. FEBS Letters 426:1-5.

80. Jones, D. M., A. Curry, and A. J. Fox. 1985. An ultrastructural study of the gastric Campylobacter-like organism 'Campylobacter pyloridis'. Journal of General Microbiology 131:2335-41.

101. Marshall, B. J., and C. S. Goodwin. 1987. Revised nomenclature of Campylobacter pyloridis. Int. J. Systematic Bacteriol. 37:68.

150. Stark, R. M., J. Greenman, and M. R. Millar. 1995. Physiology and biochemistry of Helicobacter pylori. British Journal of Biomedical Science 52:282-290.

157. Tomb, J.-F., others, and J. C. Venter. 1997. The complete genome sequence of the gastric pathogen Helicobacter pylori. Nature 388:539-547.

Anmerkungen

The source is not mentioned.

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1.1.3 Disease and epidemiology

For most of the twentieth century, peptic ulcers were thought to be stress-related and caused by hyperchlorhydria (Yoshida et al., 1977). The discovery that H. pylori is associated with gastric inflammation and peptic ulcer disease was initially met with skepticism. However, this discovery and following studies on H. pylori have revolutionized our opinion of the gastric environment, the diseases associated with it, and the appropriate treatment methods.

H. pylori is probably the most common human chronic infection and is distributed worldwide, infecting both males and females (Parkin, 2006). More than half of the world's population is persistently colonized with H. pylori. The prevalence of H. pylori is much higher in developing countries than in the Western world, although it increases with age in all populations studied (Perez-Perez et al., 2004). The incidence of H. pylori infection declines with increasing standards of socioeconomic development, including sewage disposal, water chlorination, hygienic food preparation, decreased crowding, and education (Ford et al., 2006). Natural acquisition of H. pylori infection usually occurs during childhood (Mourad-Baars and Chong, 2006). Once established, H. pylori generally persists for decades unless eradicated by anti-microbial therapy (Go, 2002; Magalhães Queiroz and Luzza , 2006). Because of the worldwide prevalence of infection, transmission of the organism from person to person is a major concern. Early studies demonstrated intra-familial clustering of infection, and more recently, DNA analyses of isolates have confirmed that most transmission occurs locally within families or small population groups ( Suerbaum et al., 1998; Drumm et al., 1990; Kivi et al., 2003). These results are consistent with an apparent inability of H. pylori to proliferate or survive for long periods in the environment. The mode of transmission from person to person has not been proven definitively. Oral-fecal, oral-oral, and gastro-oral routes are all considered possible (Magalhães Queiroz and Luzza , 2006). The study of the mode of transmission is made difficult by the fact that, unlike other infectious diseases, there is no well-defined clinical syndrome associated with its acquisition, and expression of chronic H. pylori infection in humans is highly variable. Hence, the usual approach of identifying cases and determining important exposures with infectious diseases [is not possible.]


Drumm, B., G. I. Perez-Perez, M. J. Blaser, and P. M. Sherman, Intrafamilial clustering of Helicobacter pylori infection, N Engl J Med, 322, 359-363, 1990,

Ford, A. C., D. Forman, A. G. Bailey, A. T. Axon, and P. Moavvedi, Initial poor quality of life predicts the new onset of dyspepsia: results from a longitudinal ten-year follow-up study, Gut, 2006,

Go, M. F., Review article: Natural history and epidemiology of Helicobacter pylori infection, Aliment Pharmacol Ther, 16 Suppl 1, 3-15, 2002.

Kivi, M., Y. Tindberg, M. Sorberg, T. H. Casswall, R. Befrits, P. M. Hellstrom, C. Bengtsson, L. Engstrand, and M. Granstrom, Concordance of Helicobacter pylori strains within families, J Clin Microbiol, 41, 5604-5608, 2003,

Magalhaes Queiroz, D. M., and F. Luzza, Epidemiology of Helicobacter pylori infection, Helicobacter, 11 Suppl 1, 1-5, 2006,

Parkin, D. M., The global health burden of infection-associated cancers in the year 2002, Int J Cancer, 118, 3030-3044, 2006.

Perez-Perez, G. I., D. Rothenbacher, and H. Brenner, Epidemiology of Helicobacter pylori infection, Helicobacter, 9 Suppl 1, 1-6, 2004.

Suerbaum, S., J. M. Smith, K. Bapumia, G. Morelli, N. H. Smith, E. Kunstmann, I. Dyrek, and M. Achtman, Free recombination within Helicobacter pylori, Proc Natl Acad Set USA, 95, 12,619-12,624, 1998.

Yoshida, T., H. Kubo, H. Murata, K. Ando, H. Ishii, and F. Miyagi, Acute multiple gastric ulcers in the pyloric antrum, Endoscopy, 9, 223-228, 1977,

Disease and Epidemiology

For most of the twentieth century, peptic ulcers were thought to be stress-related and caused by hyperchlorhydria. The discovery that H. pylori is associated with gastric inflammation and peptic ulcer disease was initially met with skepticism. However, this discovery and subsequent studies on H. pylori have revolutionized our view of the gastric environment, the diseases associated with it, and the appropriate treatment regimens.

H. pylori is probably the most common human chronic infection and is distributed worldwide. More than half of the world’s population is persistently colonized with H. pylori (34). The prevalence of H. pylori is much higher in emergent countries than in the Western world, although it increases with age in all populations studied (54). The incidence of H. pylori infection declines with increasing standards of socioeconomic development, including sewage disposal, water chlorination, hygienic food preparation, decreased crowding, and education (134). Once established, H. pylori generally persists for decades unless eradicated by anti-microbial therapy.

Because of the worldwide prevalence of infection, transmission of the organism from person to person is a major concern. Early studies demonstrated intrafamilial clustering of infection (42) and, more recently, DNA analyses of isolates have confirmed that most transmission occurs locally within families or small population groups (86, 153). These results are consistent with an apparent inability of H. pylori to proliferate or survive for long periods in the environment.

The mode of transmission from person to person has not been proven definitively. Oral-fecal, oral-oral, and gastro-oral routes have all been considered

[page 5]

possible (109). The study of the mode of transmission is made difficult by the fact that, unlike other infectious diseases, there is no well-defined clinical syndrome associated with its acquisition, and expression of chronic H. pylori infection in humans is highly variable. Hence, the usual approach of identifying cases and determining important exposures with infectious diseases is not possible.


34. Cover, T. L., D. E. Berg, M. J. Blaser, and H. L. T. Mobley. 2001. H. pylori pathogenesis, p. 509-558. In E. A. Groisman (ed.), Principles of Bacterial Pathogenesis. Academic Press, San Diego.

42. Drumm, B., G. I. Perez-Perez, M. J. Blaser, and P. M. Sherman. 1990. Intrafamilial clustering of Helicobacter pylori infection. New Engl. J. Med. 322:359-363.

54. Forman, D., and P. Webb. 1993. Geographic distribution and association with gastric cancer, p. 11-20. In T. C. Northfield, M. Mendall, and P. M. Goggin (ed.), Helicobacter pylori infection. Kluwer Academic Publishers, Boston.

86. Kersulyte, D., H. Chalkauskas, and D. E. Berg. 1999. Emergence of recombinant strains of Helicobacter pylori during human infection. Mol. Microbiol. 31:31-43.

109. Megraud, F. 1992. Epidemiology of Helicobacter pylori infection, p. 107-123. In B. J. Rathbone and R. V. Heatley (ed.), Helicobacter pylori and Gastroduodenal Disease, 2 ed. Blackwell Scientific Publications, Oxford.

134. Pounder, R. E., and D. Ng. 1995. The prevalence of Helicobacter pylori in different countries. Aliment. Pharmacol. Ther. 9:S33-S39.

153. Suerbaum, S., J. M. Smith, K. Bapumia, G. Morelli, N. H. Smith, E. Kunstmann, I. Dyrek, and M. Achtman. 1998. Free recombination within Helicobacter pylori. Proc. Natl. Acad. Sci. U.S.A. 95:12619-12624.

Anmerkungen

The source is not mentioned.

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Although most infections are asymptomatic, about 10% of cases of H. pylori colonization lead to illness. H. pylori is a major cause of chronic active gastritis and peptic ulcer disease and is also an early risk factor for gastric cancer. Infections are occasionally cleared spontaneously after a brief acute phase, but many last for years or decades, and it is these long-term infections that are most often implicated in disease (Kusters et al., 2006). The persistence of the H. pylori infection is surprising considering that the bacterium stimulates marked humoral and cellular immune responses in the human host, which are insufficient to clear the infection (Harry L. T. Mobley and Hazell , 2001; Suerbaum and Michetti , 2002).

1.1.4 Ecological niche

The means by which H. pylori occupies its gastric niche and the basis for its biochemical capabilities and requirements is of great fundamental interest. A thorough understanding of H. pylori physiology and metabolism could lead to new and better drug therapies, to the identification of potential targets for therapeutic intervention, or to an effective vaccine. Understanding how the organism colonizes and persists in the host is an important step in fully understanding its pathogenesis.

H. pylori have adapted to survive in the very specific and unique ecological niche of the human stomach (Lee and Josenhans, 2005; Sachs et al., 2003; Go, 2002). Because of the presence of gastric acid which rapidly destroys the majority of bacteria, the stomach is typically colonized only by transient oral flora. H. pylori appears to have evolved specific mechanisms to assist its survival in this hostile environment. These factors include the ability to swim well in the thick, protective mucus gel layer, the ability to transiently survive exposure to acid, and the ability to attach to the epithelial cell layer to prevent the bacteria from being washed out of the stomach through the mechanical action of peristalsis. As a result, other infectious agents do not appear to successfully compete with H. pylori in this environment (Sachs et al., 2003).

Major non-specific host defenses against microbial colonization of the stomach are gastric acid, peristalsis, and the continual shedding of the cells and mucus lining of the gastric surface.


Go, M. F., Review article: Natural history and epidemiology of Helicobacter pylori infection, Aliment Pharmacol Ther, 16 Suppl 1, 3-15, 2002.

Harry L. T. Mobley, G. L. M. and S. L. Hazell, Helicobacter pylori Physiology and Genetics, ASM Press, 2001,

Kusters, J. G., A. H. van Vliet, and E. J. Kuipers, Pathogenesis of Helicobacter pylori infection, Clin Microbiol Rev, 19, 449-490, 2006,

Lee, S. K,, and C. Josenhans, Helicobacter pylori and the innate immune system, Int J Med Microbiol, 295, 325-334, 2005,

Sachs, G., D. L. Weeks, K. Melchers, and D. R. Scott, The gastric biology of Helicobacter pylori, Annu Rev Physiol, 65, 349-369, 2003,

Suerbaum, S., and P. Michetti, Helicobacter pylori infection, N Engl J Med, 347, 1175-1186, 2002.

Although most infections are asymptomatic, about 10% of cases of H. pylori colonization lead to illness (34). H. pylori is a major cause of chronic active gastritis and peptic ulcer disease (80, 81, 141, 150) and is also an early risk factor for gastric cancer (127, 128). Infections are occasionally cleared spontaneously after a brief acute phase, but many last for years or decades, and it is these long-term infections that are most often implicated in disease (16, 159). The persistence of the H. pylori infection is surprising considering that the bacterium stimulates marked humoral and cellular immune responses in the human host, which are insufficient to clear the infection (26).

[page 6]

Ecological niche

The means by which H. pylori occupies its gastric niche and the basis for its biochemical capabilities and requirements is of great fundamental interest. A thorough understanding of H. pylori physiology and metabolism could lead to new and better drug therapies, to the identification of potential targets for therapeutic intervention, or to an effective vaccine. Understanding how the organism colonizes and persists in the host is an important step in fully understanding its pathogenesis.

H. pylori has adapted to survive in the very specific and unique ecological niche of the human stomach. Because of the presence of gastric acid, which rapidly destroys the majority of bacteria, the stomach is typically colonized only by transient oral flora (156). H. pylori appears to have evolved specific mechanisms to assist its survival in the hostile environment. These factors include the ability to swim well in the thick, protective mucus gel layer, the ability to transiently survive exposure to acid, and the ability to attach to the epithelial cell layer to prevent the bacteria from being washed out of the stomach through the mechanical action of peristalsis. As a result, other infectious agents do not appear to successfully compete with H. pylori in this environment.

Major non-specific host defenses against microbial colonization of the stomach are gastric acid, peristalsis, and the continual shedding of the cells and mucus lining the gastric surface (34).


16. Blaser, M. J. 1992. Perspectives on the pathogenesis of Helicobacter pylori infections, p. 276-280. In B. J. Rathbone and R. V. Heatley (ed.), Helicobacter pylori and Gastroduodenal Disease, 2nd ed. Blackwell Scientific Publishing, Oxford.

26. Chen, M., and A. Lee. 1993. Vaccination possibilities and probabilities, p. 158-169. In T. C. Northfield, M. Mendall, and P. M. Goggin (ed.), Helicobacter pylori infection. Kluwer Academic Publishers, Boston.

34. Cover, T. L., D. E. Berg, M. J. Blaser, and H. L. T. Mobley. 2001. H. pylori pathogenesis, p. 509-558. In E. A. Groisman (ed.), Principles of Bacterial Pathogenesis. Academic Press, San Diego.

80. Jones, D. M., A. Curry, and A. J. Fox. 1985. An ultrastructural study of the gastric Campylobacter-like organism 'Campylobacter pyloridis'. Journal of General Microbiology 131:2335-41.

81. Jones, D. M., A. M. Lessells, and J. Eldridge. 1984. Campylobacter like organisms on the gastric mucosa: culture, histological, and serological studies. Journal of Clinical Pathology 37:1002-6.

127. Nomura, A., G. N. Stemmermann, P.-H. Chyou, I. Kato, G. I. Perez- Perez, and M. J. Blaser. 1991. Helicobacter pylori infection and gastric carcinoma among Japanese Americans in Hawaii. The New England Journal of Medicine 325:1132-6.

128. Parsonnet, J., G. D. Friedman, D. P. Vandersteen, Y. Chang, J. H. Vogelman, N. Orentreich, and R. K. Sibley. 1991. Helicobacter pylori infection and the risk of gastric carcinoma. The New England Journal of Medicine 325:1127-31.

141. Rollason, T. P., J. Stone, and J. M. Rhodes. 1984. Spiral organisms in endoscopic biopsies of the human stomach. Journal of Clinical Pathology 37:23- 6.

150. Stark, R. M., J. Greenman, and M. R. Millar. 1995. Physiology and biochemistry of Helicobacter pylori. British Journal of Biomedical Science 52:282-290.

156. Thompkins, D. S. 1992. Isolation and characterization of Helicobacter pylori, p. 19-28. In B. J. Rathbone and R. V. Heatley (ed.), Helicobacter pylori and Gastroduodenal Disease, 2 ed. Blackwell Scientific Publications, Oxford.

159. Tytgat, G., and M. Dixon. 1993. Overview: Role in peptic ulcer disease, p. 75-87. In T. C. Northfield, M. Mendall, and P. M. Goggin (ed.), Helicobacter pylori infection. Kluwer Academic Publishers, Boston.

Anmerkungen

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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.

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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.

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Therefore, the presence or absence of the cag PAI is an important characteristic among H. pylori strains.

Additional strain-specific genes have been identified by comparing the complete genome sequences of H. pylori 26695 with H. pylori J99 (Alm and Trust , 1999). The overall genomic organization, gene order and predicted proteomes (sets of proteins encoded by the genome) were found to be quite similar. Both strains contained the complete cag PAI flanked by the same chromosomal genes and a previously described 31-bp repeat (Akopyants et al., 1998; Censini et al., 1996). The DNA-sequence differences between orthologues from the two strains are found mainly in the third position of coding triplets, consistent with the variation seen between H. pylori strains identified by methods dependent on the nucleotide sequence or on the sequencing of specific loci in different strains (Akopyanz [sic] et al., 1992). This nucleotide variation however does not translate into a highly divergent proteome. A total of 275 (18.4%) J99 and 290 (18.7%) 26695 gene products have orthologues of unknown function in other species, and 346 (23.1%) J99 and 367 (23.6%) 26695 genes are H. pylori specific, showing no sequence similarity with genes available in public databases. Of these H. pylori specific genes, 56 and 69 are specific to strains J99 and 26995, respectively (Alm et al., 1999).

The fact that strain-specific DNA-restriction/modification genes have a lower (G+C) content than the remainder of the genome and are associated with regions that are organized differently in the J99 and 26695 genomes indicates that these genes may have been acquired horizontally from other bacterial species or transferred more recently from other H. pylori strains by natural transformation (Alm et al., 1999).


Alm, R. A., and T. J. Trust, Analysis of the genetic diversity of Helicobacter pylori: the tale of two genomes, J Mol Med, 77, 834-846, 1999.

Alm, R. A., L. S. Ling, D. T. Moir, B. L. King, E. D. Brown, P. C. Doig, D. R. Smith, B. Noonan, B. C. Guild, B. L. deJonge, G. Carmel, P. J. Tummino, A. Caruso, M. Uria-Nickelsen, D. M. Mills, C. Ives, R. Gibson, D. Merberg, S. D. Mills, Q. Jiang, D. E. Taylor, G. F. Vovis, and T. J. Trust, Genomic-sequence comparison of two unrelated isolates of the human gastric pathogen Helicobacter pylori, Nature, 397, 176-180, 1999.

Akopyanz, N., N. O. Bukanov, T. U. Westblom, S. Kresovich, and D. E. Berg, DNA diversity among clinical isolates of Helicobacter pylori detected by PCR-based rapd fingerprinting, Nucleic Acids Res, 20, 5137-5142, 1992.

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, Analyses of the cag pathogenicity island of Helicobacter pylori, Mol Microbiol, 28, 37-53, 1998.

Censini, S., C. Lange, Z. Xiang, J. E. Crabtree, P. Ghiara, M. Borodovsky, R. Rappuoli, and A. Covaeci, cag. a pathogenicity island of Helicobacter pylori, encodes type I-specific and disease-associated virulence factors, Proc Natl Acad Sci USA, 93, 14,648-14,653, 1996.

Therefore, the presence or absence of the cag PAI is an important characteristic among H. pylori strains.

[page 12]

Additional strain-specific genes have been identified by comparing the complete genome sequences of H. pylori 26695 with H. pylori J99 (7). The overall genomic organization, gene order and predicted proteomes (sets of proteins encoded by the genome) were found to be quite similar. Both strains contained the complete cag PAI flanked by the same chromosomal genes and a previously described 31-bp repeat (2). The DNA-sequence differences between orthologues from the two strains are found mainly in the third position of coding triplets, consistent with the variation seen between H. pylori strains identified by methods dependent on the nucleotide sequence or on the sequencing of specific loci in different strains (1). However, this nucleotide variation does not translate into a highly divergent proteome. A total of 275 (18.4%) J99 and 290 (18.7%) 26695 gene products have orthologues of unknown function in other species, and 346 (23.1%) J99 and 367 (23.6%) 26695 genes are H. pylori specific, showing no sequence similarity with genes available in public databases. Of these H. pylori specific genes, 56 and 69 are specific to stains J99 and 26995, respectively (7).

[page 13]

The fact that strain-specific DNA-restriction/modification genes have a lower (G+C) content than the remainder of the genome and are associated with regions that are organized differently in the J99 and 26695 genomes indicates that these genes may have been acquired horizontally from other bacterial species or transferred more recently from other H. pylori strains by natural transformation (7).


1. Akopyants, N., N. O. Bukanov, T. U. Westblom, S. Kresovich, and D. E. Berg. 1992. DNA diversity among clinical isolates of Helicobacter pylori deteted [sic] by PCR-based RAPD fingerprinting. Nucleic Acids Res. 20:5137-5142.

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.

7. Alm, R., L.-S. L. Ling, D. T. Moir, B. L. King, E. D. Brown, P. C. Doig, D. R. Smith, B. Noonan, B. C. Guild, B. L. deJonge, G. Carmel, P. J. Tummino, A. Caruso, M. Uria-Nickelsen, D. M. Mills, C. Ives, R. Gibson, D. Merberg, S. D. Mills, Q. Jiang, D. E. Taylor, G. F. Vovis, and T. J. Trust. 1999. Genomic-sequence comparison of two unrelated isolates of the human gastric pathogen Helicobacter pylori. Nature 397:176-180.

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There is increasing evidence that recombination occurs between different H. pylori strains (Kraft et al., 2006; Kraft and Suerbaum, 2005; Suerbaum and Achtman, 2004). Simultaneous colonization of human stomachs with more than one strain of H. pylori is detectable in about 5-10% of patients in the United States (Fujimoto et al., 1994), and may occur even more commonly in other populations (Jorgensen et al., 1996). Mixed infections, even those that are transient, provide an opportunity for genetic exchange between strains. Analysis of single cell clones from a patient who was naturally infected with two different H. pylori strains, one of which was cag+ and the other cag-, revealed evidence for at least six different genetic exchanges. One of these exchanges resulted in the replacement of the entire cag PAI with DNA containing the empty site allele from the cag-negative strain. Several others involved a region encoding putative outer membrane proteins that could be involved in interactions with the host (Kersulyte et al., 1999). Genetic exchange may play an important role in the biology of H. pylori by generating new genotypes much more rapidly than is possible by mutation alone, therefore allowing cells to rapidly adapt to new sites in the gastric environment or to new hosts. For several genes, including flaA, flaB, and portions of vacA, phylogenetic analyses of orthologous sequences from different strains have yielded a bush-like rather than a tree-like pattern, indicating considerable interstrain recombination. Recombination is thought to occur more commonly in H. pylori than in any other bacterial species analyzed thus far (Suerbaum et al., 1998). Thus, the high level of allelic variation observed in H. pylori can be attributed to at least two factors. First, large populations of H. pylori have probably evolved within millions of individual human stomachs over thousands of years, resulting in considerable mutational diversity. Second, additional diversity has accumulated as a result of extensive intragenic recombination due to mixed infections (Kraft and Suerbaum, 2005).

Fujimoto, S., B. Marshall, and M. J. Blaser, PCR-based restriction fragment length polymorphism typing of Helicobacter pylori, J Clin Microbiol, 32, 331-334, 1994.

Jorgensen, M., G. Daskalopoulos, V. Warburton, H. M. Mitchell, and S. L. Hazell, Multiple strain colonization and metronidazole resistance in Helicobacter pylori-infected patients: identification from sequential and multiple biopsy specimens, J Infect Dis, 174, 631-635, 1996.

Kersulyte, D., H. Chalkauskas, and D. E. Berg, Emergence of recombinant strains of Helicobacter pylori during human infection, Mol Microbiol, 31, 31-43, 1999.

Kraft, C., and S. Suerbaum, Mutation and recombination in Helicobacter pylori: mechanisms and role in generating strain diversity, Int J Med Microbiol, 295, 299-305, 2005.

Kraft, C., A. Stack, C. Josenhans, E. Niehus, G. Dietrich, P. Correa, J. G. Fox, D. Falush, and S. Suerbaum, Genomic changes during chronic Helicobacter pylori infection, J Bacteriol, 188, 249-254, 2006.

Suerbaum, S., and M. Achtman, Helicobacter pylori: recombination, population structure and human migrations, Int J Med Microbiol, 294, 133.139, 2004.

Suerbaum, S., J. M. Smith, K. Bapumia, G. Morelli, N. H. Smith, E. Kunstmann, I. Dyrek, and M. Achtman, Free recombination within Helicobacter pylori, Proc Natl Acad Sci U S A, 95, 12,619-12,624, 1998.

[Page 13]

There is increasing evidence that recombination occurs between different H. pylori strains (10, 58, 61). Simultaneous colonization of human stomachs with more than one strain of H. pylori is detectable in about 5-10% of patients in the United States (57), and may occur even more commonly in other populations (82). Mixed infections, even those that are transient, provide an opportunity for genetic exchange between strains. Analysis of single cell clones from a patient who was naturally infected with two different H. pylori strains, one of which was cag+ and the other cag-, revealed evidence for at least six different genetic exchanges. One of these exchanges resulted in the replacement of the entire cag PAI with DNA containing the “empty site allele” from the cag-negative strain. Several others involved a region encoding putative outer membrane proteins that could be involved in interactions with the host (86). Genetic exchange may play an important role in the biology of H. pylori by generating new genotypes much more rapidly than is possible by mutation alone, therefore allowing cells to rapidly adapt to new sites in the gastric environment or to new hosts.

For several genes, including flaA, flaB, and portions of vacA, phylogenetic analyses of orthologous sequences from different strains have yielded a “bush”-like rather than a “tree”-like pattern, indicating considerable interstrain recombination. Recombination is thought to occur more commonly in H. pylori than in any other

[Page 14]

bacterial species analyzed thus far (153). Thus, the high level of allelic variation observed in H. pylori can be attributed to at least two factors. First, large populations of H. pylori have probably evolved within millions of individual human stomachs over thousands of years, resulting in considerable mutational diversity. Second, additional diversity has accumulated as a result of extensive intragenic recombination due to mixed infections (34).


10. Atherton, J. C., P. Cao, J. R. M. Peek, M. K. R. Tummuru, M. J. Blaser, and T. L. Cover. 1995. Mosaicism in vacuolating cytotoxin alleles of Helicobacter pylori. Association of specific vacA types with cytotoxin production and peptic ulceration. J. Biol. Chem. 270:17771-17777.

34. Cover, T. L., D. E. Berg, M. J. Blaser, and H. L. T. Mobley. 2001. H. pylori pathogenesis, p. 509-558. In E. A. Groisman (ed.), Principles of Bacterial Pathogenesis. Academic Press, San Diego.

57. Fujimoto, S., B. Marshall, and M. J. Blaser. 1994. PCR-based restriction fragment length polymorphism typing of Helicobacter pylori. J. Clin. Microbiol. 34:331-334.

58. Garner, J. A., and T. L. Cover. 1995. Analysis of genetic diversity in cytotoxin-producing and non-cytotoxin-producing Helicobacter pylori strains. J. Infect. Dis. 172:290-293.

61. Go, M. F., V. Kapur, D. Y. Graham, and J. M. Musser. 1996. Population genetic analysis of Helicobacter pylori by multilocus enzyme electrophoresis: Extensive allelic diversity and recombinational population structure. J. Bacteriol. 178:3934-3938.

82. Jorgensen, M., G. Daskalopoulos, V. Warburton, H. M. Mitchell, and S. L. Hazell. 1996. Multiple strain colonization and metronidazole resistance in Helicobacter pylori-infected patients: Identification from sequential and multiple biopsy specimens. J. Infect. Dis. 174:631-635.

86. Kersulyte, D., H. Chalkauskas, and D. E. Berg. 1999. Emergence of recombinant strains of Helicobacter pylori during human infection. Mol. Microbiol. 31:31-43.

153. Suerbaum, S., J. M. Smith, K. Bapumia, G. Morelli, N. H. Smith, E. Kunstmann, I. Dyrek, and M. Achtman. 1998. Free recombination within Helicobacter pylori. Proc. Natl. Acad. Sci. U.S.A. 95:12619-12624.

Anmerkungen

Although identical, nothing has been marked as a citation; the source is not given.

S. Suerbaum has been the advisor for this PhD-Thesis, thus the preference for literary references with him as author or co-author instead of the original references.

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As with several other bacterial species, including Neisseria spp. and Streptococcus pneumoniae, H. pylori is naturally competent for genetic transformation in vitro (Nedenskov-Sorensen et al., 1990). This property allows for the uptake of exogenous DNA, which may subsequently replicate, in the case of plasmids, or incorporate into the chromosome by homologous recombination. In addition to genetic exchange via transformation, H. pylori strains may exchange DNA via a contact-dependent mechanism resembling bacterial conjugation.

Nedenskov-Sorensen, P., G. Bukholm, and K. Bovre, Natural competence for genetic transformation in Campylobacter pylori, J Infect Dis, 161, 365-366, 1990.

As with several other bacterial species, including Neisseria spp. and Streptococcus pneumoniae, H. pylori is naturally competent for genetic transformation in vitro (125). This property allows for the uptake of exogenous DNA, which may subsequently replicate, in the case of plasmids, or incorporate into the chromosome by homologous recombination. In addition to genetic exchange via transformation, H. pylori strains may exchange DNA via a contact-dependent mechanism resembling bacterial conjugation (89).

89. Kuipers, E. J., D. A. Israel, J. G. Kusters, and M. J. Blaser. 1998. Evidence for a conjugation-like mechanism of DNA transfer in Helicobacter pylori. J. Bacteriol. 180:2901-2905.

125. Nedenskov-Sorensen, P., G. Bukholm, and K. Bovre. 1990. Natural competence for genetic transformation in Campylobacter pylori. J. Infect. Dis. 161:365-366.

Anmerkungen

Although identical, nothing has been marked as a citation; the source is not given.

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