Editing Peptic ulcer disease (section)

===''H. pylori''===
''[[Helicobacter pylori]]'' is one of the major causative factors of peptic ulcer disease. It secretes [[urease]] to create an alkaline environment, which is suitable for its survival. It expresses blood group antigen-binding adhesin (BabA) and outer inflammatory protein adhesin (OipA), which enables it to attach to the gastric epithelium. The bacterium also expresses virulence factors such as ''CagA'' and ''PicB'', which cause stomach mucosal inflammation. The VacA gene encodes for vacuolating cytotoxin, but its mechanism of causing peptic ulcers is unclear. Such stomach mucosal inflammation can be associated with [[hyperchlorhydria]] (increased stomach acid secretion) or [[hypochlorhydria]] (reduced stomach acid secretion). Inflammatory [[cytokine]]s inhibit the [[parietal cell]] acid secretion. ''H. pylori'' also secretes certain products that inhibit [[hydrogen potassium ATPase]]; activate [[calcitonin gene-related peptide]] sensory neurons, which increases [[somatostatin]] secretion to inhibit acid production by parietal cells; and inhibit [[gastrin]] secretion. This reduction in acid production causes gastric ulcers.<ref name="Angel 2017"/> On the other hand, increased acid production at the [[pyloric antrum]] is associated with duodenal ulcers in 10% to 15% of ''H. pylori'' infection cases. In this case, somatostatin production is reduced and gastrin production is increased, leading to increased [[histamine]] secretion from the [[enterochromaffin]] cells, thus increasing acid production. An acidic environment at the antrum causes [[metaplasia]] of the duodenal cells, causing duodenal ulcers.<ref name="Angel 2017"/>

Human immune response toward the bacteria also determines the emergence of peptic ulcer disease. The human IL1B gene encodes for [[Interleukin 1 beta]], and other genes that encode for [[tumour necrosis factor]] (TNF) and [[Lymphotoxin alpha]] also play a role in gastric inflammation.<ref name="Angel 2017"/>