Pathogenomics of Gastric and Enterohepatic Helicobacter Species

Sebastian Suerbaum, Sandra Schwarz, and ChristineJosenhans 14.1


The genus Helicobacter currently comprises 23 validly named species. These can be subdivided into the gastric Helicobacter species, which colonize the mucosa of the stomach of their host organisms, and the enterohepatic Helicobacter species, which colonize the gut and/or the liver. In addition to the fact that the type species of the genus Helicobacter, H. pylori, is one of the most prevalent human pathogens and the only recognized bacterial carcinogen [1], there are multiple other reasons why this genus is of interest in the context of pathogenomics. These bacteria are well adapted to their hosts, causing chronic or life-long infection or colonization. Most species have a very narrow host spectrum, and lack an environmental reservoir. The genus Helicobacter thus offers the possibility to use comparative geno-mics to address questions relating to host adaptation, tissue tropism, or coevolu-tion with diverse hosts, to name but a few.

H. pylori was the sixth bacterial species to have its complete genome sequence published [2], and in 1999 became the first bacterial species for which two complete sequences from unrelated strains were publicly available [3]. However, to date there is only one other member of the genus Helicobacter, H. hepaticus, whose genome sequence is known [4], so that still only limited conclusions from these comparisons are possible. Several genome projects are in progress. These include additional strains of H. pylori, either associated with specific diseases (e.g., MALT lymphoma) or belonging to specific populations of H. pylori, such as the hpAfrica2 population [5]. They also include other Helicobacter species, such as the ferret stomach pathogen, H. mustelae. While the basis for genomic comparisons is currently limited to three genomic sequences from two Helicobacter species, the comparisons with the closely related species Campylobacter jejuni [6] and Wolinella succinogenes [7] are likewise of interest. We will also include in this review the results of studies that have addressed the variability of Helicobacter genomes using microarray hybridizations, and studies concerned with the global variability of H. pylori and its relationship to disease.

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Helicobacter pylori

H. pylori is a widespread human pathogen that colonizes the gastric mucosa, where it persists unless eradicated by specific therapy. Infection is usually acquired in childhood and always leads to an infiltration of the mucosa with neutrophils and lymphocytes (chronic active gastritis). While this infection remains asymptomatic in approx. 85% of cases, it can lead to peptic ulceration of the duodenum or the stomach, to gastric cancer, or to gastric lymphoma of the mucosa-associated lymphoid tissue (for a general review on H. pylori, see Ref. [1]). Since its discovery in 1982 [8], this species has been studied extensively, but many features of the pathogenic lifestyle remain obscure, and the clinical outcome of infection still cannot be predicted from either bacterial or host genetic markers.

The complete genomic sequences of two unrelated H. pylori isolates, 26695 and J99, were published by The Institute of Genomic Research (TIGR) and the pharmaceutical company AstraZeneca in 1997 and 1999, respectively [2, 3]. The genomes of the H. pylori strains 26695 and J99 are single circular chromosomes respectively 1.67 Mbp and 1.64 Mbp in size and with a G+C content of 39%. The two genome sequences have been analyzed in great detail with respect to the physiology and metabolic capabilities of H. pylori [9, 10].

The early availability of the complete genome sequence has had a tremendous impact on H. pylori research and is largely responsible for the rapid progress made in the analysis of H. pylori pathogenesis over the last 8 years.

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