Helicobacter pyloriBabA in adaptation for gastric colonization

Abstract

Helicobacter pylori (H. pylori) as a causative agent of gastric complications, is well adapted for the colonization of gastric mucosa. Although the infectious process depends on several factors, the adhesion to the gastric mucosa is the first and important step. Among several outer membrane proteins, BabA is one of the significant protein involving in many inflammatory processes in addition to its role in the attachment for the persistent colonization. We performed a PubMed search using the key words: “babA”, “pylori”, “gastric complications”, “homologous recombination”, “slipped strand mispairing”; a total of 249 articles were displayed. Of these we mainly focused on articles with the full text in English and published between 2005 and 2016. H. pylori BabA is involved in binding with receptors; however, its synthesis is regulated by phase variation. In this review we confirm that H. pylori babA can be modulated at the molecular and functional levels to adapt to the stress within the gastro-intestinal tract.

Helicobacter pylori pathogenicity and primary antimicrobial resistance in Northern Spain

“…Indeed, the cagA/vacAs1m1 genotype was found in 20.6% isolates from patients of mild-vs 54.5% from severe-disease group, which agrees with the association between this genotype and the higher pathogenicity. 11 Prevalence of babA2 varies widely among different populations; from 35%-60% in Europe to 100% in Asia, 11,31 most of our isolates were positive for babA2 (>94%) but we could not know if the protein was expressed or not, further studies should be done in order to know if posttranscriptional modification occurred. 30 Infection experiments showed that 22.2% cagA-positive strains were unable to translocate CagA into the host cells, showing non-expression of cagA or a non-functionality of the cag-T4SS of these strains.…”

“…Antibiotic susceptibility testing should be performed prior to therapy and regional surveillance of primary antibiotic resistance of H pylori is recommended. 11,12 The functional status of OipA is regulated by slipped-strand mispairing that is determined by the number of CT dinucleotide repeats in the 5´region of the gene (status ON is functional and OFF is nonfunctional). Several factors contribute to this situation such as environmental parameters, host genetic susceptibility and bacteria virulence factors.…”

“…10 Although 50% of human population is infected by H pylori, only a fraction of individuals develops gastric diseases. 11 Another virulence factor of H pylori is the duodenal ulcer promoting gene (dupA). 4,5 The two best-studied virulence factors associated with the development of gastric cancer (GC) are the CagA and VacA proteins.…”

“…5 Other virulence factors are the outer membrane proteins, BabA (blood group antigen binding adhesion) and OipA (outer inflammatory protein) involved in the adhesion to the gastric mucosa. 11,12 The functional status of OipA is regulated by slipped-strand mispairing that is determined by the number of CT dinucleotide repeats in the 5´region of the gene (status ON is functional and OFF is nonfunctional). 11 Another virulence factor of H pylori is the duodenal ulcer promoting gene (dupA).…”

Tipping the Scale Towards Gastric Disease: a Host-Pathogen Genomic Mismatch?

“…Through co-evolution, chronic pathogens with vertical or familial transmission become less virulent over time [89–93], and H. pylori infections are well tolerated by humans, causing low-grade inflammation and possibly protecting against allergic and related disorders [25–29, 94, 95]. The H. pylori gene babA2 demonstrates adaptive microevolution with humans [96]. BabA binds blood group antigens and triggers pro-inflammatory cytokine release.…”