Helicobacter pylori
A Microbial Biorealm page on the genus Helicobacter pylori
Classification
Higher order taxa
Bacteria (Domain); Proteobacteria (Phylum); Epsilon Proteobacteria (Class); Campylobacterales (Order); Helicobacteraceae (Family); Helicobacter (Genus)
Species
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NCBI: Taxonomy |
Helicobacter pylori
Description and significance
Helicobacter pylori is a Gram negative organism that has a helical or spiral shaped with 6-8 flagella at one end. The size of the organism measures about 2-4 μm x 0.5-1.0 μm. H. pylori is found in a very acidic environment, a pH of 2.0 or less. It is cultured in microaerobic (low oxygen conditions) but it adapts to high oxygen at high culture densities. It is commonly found inside the lining of the stomach and the duodenum. H. pylori is a slow growing organism that can cause peptic ulcers and gastritis that can lead to gastric cancer and gastric MALT lymphoma (mucosa-associated lyphoid tissue).
It was first observed in 19th century that curved bacteria were living in the lining of the stomach, but growing and isolating the bacteria was neglected. H. pylori was isolated in Perth, Western Australia by Barry Marshall and Robin Warren in 1983. They discovered that H. pylori was related to peptic ulcers. To prove this evidence, the organism was cultured from the stomach, and concluded that H. pylori was the bacteria that caused peptic ulcers and gastritis. [2] In 2005, Marshall and Warren received the Nobel Prize in physiology or medicine for their discovery of the Helicobacter pylori. [4]
Helicobacter pylori was initially named Campylobacter pylordis because it appeared that the organism was similar to other Campylobacters, it showed similar appearances with the campylobacter jejuni. Using rRNA hybridation sequencing, H. pylori was shown that it was different from the Campylobacter genus. H.pylori was separated into its own genus Helicobacter in 1989. The Helicobacter reflects to the appearances of the organism, helical in vivo, but often rodlike in vitro. [Marshall]
Genome structure
The two strains of the genomes have been completely sequenced. H. pylori 26695 and J99. Both were sequenced using a random shotgun approaching from libraries of cloned chromosonal fragments of ~2.5kb. The 26695 genome was 24kb larger than the J99, but both of the genomes had G+C% of 39%. Both genomes had similar average lenths of coding sequences, coding density and the bias of initiation codons. The orgin of replication of the genome J99 was not clearly identifiable.
The genome of Helicobacter pylori strain "26695" is circular and contains 1,667,867 base pairs, and strain "J99" contains 1,643,831 base pairs. 300 bp encodes for membrane proteins, and 1590 bp are predicted coding sequences. The chromosome of the organism contains genes that encodes the urease gene cluster, cytotoxins in the membrane, and the cag pathogenicity island. In 1989, CagA gene was found and identified as the marker strain of the risk of peptic ulcers and gastric cancer. The CagA pathogenicity island recognizes the type IV secretion system, which CagA proteins are moved to the host cells. [1]
The DNA content of H. pylori has GC range of 35-38% which catergorized itself to the Campylobacter species. However, the comparisons of the 16S ribosomal RNA showed that H. pylori was different from Campylobacter but similar to Wolinella succinogenes. which its GC range was 42-49%. H. pylori was placed into its own genus, Helicobacter. after the analysis of the ultrastructure, fatty acid composition and biochemical tests which proved different for H. pylori and W. succinogenes [Marshall]
The analysis of H. pylori sequences specifies the diversity and the development of the organism. H. pylori sequences shows that the recombination and the clone between the strain linkage is uncertain, and the recombination is based on the repetitive DNA sequences that permits the high frequency deletion and duplication of the DNA. The genome contains sequences that encodes for the membrane proteins. For example, the F1F0 ATP synthase complex, various oxidoreductases such as cytochrome o, and some transporters. [Modlin] Sequences show that H. pylori obtains a “well developed systems for motility, for scavenging iron, and for DNA restriction and modification.” [4] Helicobacter pylori are capable to uptake DNA from other H. pylori. Due to the uncertainty of the strain linkages, recombination occurs because of the repetitive DNA squences, which allows high frequency deletion and duplication and mismatch inbetween the strands. Lack of mismatch repairing can increase in frequency of random variation but it can also convert the gene which can bring down the diversity of the organism. [1]
Cell structure and metabolism
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Ecology
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Pathology
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Application to Biotechnology
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Current Research
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References
[1] Blaser, Martin J and Atherton, John C."Helicobacter pylori persistence: biology and disease". J Clin Invest. 2004 February 1; 113(3): 321–333.
Marshall, Barry J, McCallum, Richard W and Guerrant, Richard L. "Helicobacter pylori in peptic ulceration and gastritis." Blackwell Scientific Publications 1991; 24-25
Megraud, F. "Taxonomy and Biology of Helicobacter pylori- a comment". "Helicobacter pylori, Gastritis and Peptic Ulcer". Springer-Verlag Berlin Heidelberg 1990; 59
Modlin, Irvin M. and Sachs, George. "Acid Related Diseases, Biology and treatment" Lippincott Williams and Wilkins 2004; 461-462
[2] NCBI Entrez Genome Project
[3] The Nobel Prize in Physiology or Medicine 2005 awarded to Barry J. Marshall and J. Robin Warren "for their discovery of the bacterium Helicobacter pylori and its role in gastritis and peptic ulcer disease".
[4] Tomb JF, White O, Kerlavage AR, Clayton RA, Sutton GG, Fleischmann RD, Ketchum KA, Klenk HP, Gill S, Dougherty BA, Nelson K, Quackenbush J, Zhou L, Kirkness EF, Peterson S, Loftus B, Richardson D, Dodson R, Khalak HG, Glodek A, McKenney K, Fitzegerald LM, Lee N, Adams MD, Hickey EK, Berg DE, Gocayne JD, Utterback TR, Peterson JD, Kelley JM, Cotton MD, Weidman JM, Fujii C, Bowman C, Watthey L, Wallin E, Hayes WS, Borodovsky M, Karp PD, Smith HO, Fraser CM, Venter JC. "The complete genome sequence of the gastric pathogen Helicobacter pylori." Nature 1997. 388(6642): 515-6
Edited by Katherine Park student of Rachel Larsen and Kit Pogliano
