Chronic gastritis and gastric ulcers is infection by heliobacter pylori

H. pylori disturb proteins of tight junction – this can lead to ulcers.

Strong association between infection with H. Pylori and gastric carcinoma

H. pylori disrupts the zonula occludens (tight junction) by associating with the proteins of the junction and compromising their barrier function.

Cancerous cells typically lack gap junctions, these cells are unable to communicate or interact intercellulary, which would regulate their activities.

The gap junction defect can result in controlled mitotic activity and tumor growth.

- If the normal protective barrier of the stomach is damaged, the presence of H+ and pepsin may injure the gastric mucosa
- A major causative factor in the development of a gastric ulcer is Heliobacter pylori infection.  H. pylori has high urease activity and converts urea to NH4+, which damages the gastric mucosa.
- H+ secretion is decreased, not increased (as might be assumed).
- Gastrin levels are increased (by negative feedback) in patients with gastric ulcer disease b/c of lower-than-normal H+ secretion.