Helicobacter pylori is a gram-negative, microaerophilic bacterium that infects various areas of the stomach and duodenum. Many cases of peptic ulcers, gastritis, duodenitis, and cancers are caused by H. pylori infections. However, many who are infected do not show any symptoms of disease. H. pylori's helical shape (from which the genus name is derived) is thought to have evolved to penetrate and favor its motility in the mucus gel layer.

H. pylori is a helical shaped Gram-negative bacterium, about 3 micrometres long with a diameter of about 0.5 micrometre. It has 4–6 flagella. It is microaerophilic, i.e. it requires oxygen but at lower levels than those contained in the atmosphere. It contains a hydrogenase which can be used to obtain energy by oxidizing molecular hydrogen (H₂) that is produced by other intestinal bacteria.It tests positive for oxidase, catalase, and urease. It is capable of forming biofilms and conversion from helical to coccoid form, both likely to favor its survival and be factors in the epidemiology of the bacterium. The coccoid form of the organism has not been cultured, but has been found in the water supply in the US. This form has also been found to be able to adhere to gastric epithelial cells in vitro.

The medical community was slow to recognize the role of this bacterium in stomach ulcers and gastritis, believing that no microorganism could survive for long in the acidic environment of the stomach.  There is experimental evidence, however, to show that Heliobacter species are not, in fact transmitted via the fecal-oral route, but rather through oral-oral contact.  H. pylori is a contagious bacterium. Many researchers think that H. pylori is transmitted orally by means of fecal matter through the ingestion of waste tainted food or water. A clean and hygienic environment can help decrease the risk of H. pylori infection.

With its flagella, the bacterium moves through the stomach lumen and drills into the mucus gel layer of the stomach. It then finds ways to live in various areas of the stomach. The known areas include: inside the mucus gel layer (with a preference for the superficial area), above epithelial cells, and inside vacuoles formed by H. pylori in epithelial cells. It produces adhesins which bind to membrane-associated lipids and carbohydrates and help its adhesion to epithelial cells. An example of this is the Lewis b antigen. It produces large amounts of urease enzymes which are localized inside and outside of the bacterium. Urease metabolizes urea (which is normally secreted into the stomach) to carbon dioxide and ammonia (which neutralizes gastric acid). The survival of H. pylori in the acidic stomach is dependent on urease, and it would eventually die without it. The ammonia that is produced is toxic to the epithelial cells, and, along with the other products of H. pylori—including protease, catalase and certain phospholipases—causes damage to those cells.

Two related mechanisms by which H. pylori could promote cancer are under investigation. One mechanism involves the enhanced production of free radicals near H. pylori and an increased rate of host cell mutation. The other proposed mechanism has been called a "perigenetic pathway" and involves enhancement of the transformed host cell phenotype by means of alterations in cell proteins such as adhesion proteins. It has been proposed that H. pylori induces inflammation and locally high levels of TNF-alpha and/or interleukin 6. According to the proposed perigenetic mechanism, inflammation-associated signaling molecules such as TNF-alpha can alter gastric epithelial cell adhesion and lead to the dispersion and migration of mutated epithelial cells without the need for additional mutations in tumor suppressor genes such as genes that code for cell adhesion proteins.