Helicobacter pylori infections are common and usually have no symptoms. In 2015 it was estimated that more than 50% of the world's population is colonized by the bacterium. However, in 10-20% of the cases an infection results in gastritis (stomach inflammation) or ulcers. In some cases the infection may lead to the development of certain cancers [Blaser06]. Pathogenicity is correlated with the presence of pathogenicity islands in the genome [Broutet01, Miehlke01, Baldwin07, ZawilakPawlik19]. However, disease outcome depends on additional factors, such as the host's physiology, genotype and dietary habits.

Helicobacter pylori was discovered only in 1982 [Warren83, Marshall84]. It is highly motile owing to four to six flagella. While it is a heterotroph, it can also produce energy by oxidizing molecular hydrogen (H₂) produced by other intestinal bacteria [Olson02]. It produces large amounts of the ammonia-producing enzyme urease, which helps it overcome the stomach acidity. Its O antigen (external part of the lipopolysaccharide) is often fucosylated to mimic the Lewis blood group antigens found on the human gastric epithelium [Kusters06].

Helicobacter pylori 26695, originally known as Campylobacter pyloridis NE 26695, was isolated in 1986 from a human gastric biopsy of a patient in Southampton, England, as part of the collection of Dr D.R. Morgan from Norwich Eaton Pharmaceuticals Inc. [Morgan87, Morgan87a, Leunk88]. The genome of Helicobacter pylori 26695 was originally sequenced in 1997 [Tomb97]. This Pathway/Genome Database (PGDB) was generated by the PathoLogic component [Karp11] of the Pathway Tools software version 25.5 [Karp16] and MetaCyc version 25.5 [Caspi18] on 21 Jun 2021, using a genome annotation by RefSeq that was generated on 02 Apr 2021. The database was subsequently upgraded by limited manual curation.