Helicobacter pylori
From DrugPedia: A Wikipedia for Drug discovery
Helicobacter pylori
It is a Gram-negative, microaerophilic bacterium that can inhabit various areas of the stomach, particularly the antrum.
Kingdom | Bacteria |
---|---|
Phylum | Proteobacteria |
Class | Epsilonproteobacteria |
Order | Campylobacterales |
Family | Helicobacteraceae |
Genus | Helicobacter |
Species | H. pylori |
Binomial | Helicobacter pylori |
Surface Characteristics
H. pylori possesses five major outer membrane protein (OMP) families. The largest family includes known and putative adhesins. The other four families include porins, iron transporters, flagellum-associated proteins and proteins of unknown function. Like other typical Gram-negative bacteria, the outer membrane of H. pylori consists of phospholipids and lipopolysaccharide (LPS). The O antigen of LPS may be fucosylated and mimic Lewis blood group antigens found on the gastric epithelium. The outer membrane also contains cholesterol glucosides, which are found in few other bacteria. H. pylori has 4-6 lophotrichous flagella; all gastric and enterohepatic Helicobacter species are highly motile due to flagella. The characteristic sheathed flagellar filaments of Helicobacter are composed of two copolymerized flagellins, FlaA and FlaB.
Pathogenic Activity
It causes a chronic low-level inflammation of the stomach lining and is strongly linked to the development of duodenal and gastric ulcers and stomach cancer. Over 80% of individuals infected with the bacterium are asymptomatic.
Virulence
H. pylori is also found on the inner surface of the stomach epithelial cells and occasionally inside epithelial cells. It produces adhesins which bind to membrane-associated lipids and carbohydrates and help it adhere to epithelial cells. For example, the adhesin BabA binds to the Lewis b antigen displayed on the surface of stomach epithelial cells. H. pylori produces large amounts of the enzyme urease, molecules of which are localized inside and outside of the bacterium. Urease breaks down urea (which is normally secreted into the stomach) to carbon dioxide and ammonia. The ammonia is converted to ammonium by taking a proton (H+) from water, which leaves only a hydroxyl ion. Hydroxyl ions then react with carbon dioxide, producing bicarbonate which neutralizes gastric acid. The survival of H. pylori in the acidic stomach is dependent on urease. The ammonia produced is toxic to the epithelial cells, and, along with the other products of H. pylori—including proteases, vacuolating cytotoxin A (VacA), and certain phospholipases—damages those cells.