Helicobacter pylori was the first, formally recognized bacterial pathogen and one of the most successful. Estimates predict that over half of the world’s population suffer from various levels of H. pylori colonization and infection.

Pathophysiology:

Colonization of this bacterium is almost always associated with active gastritis. The condition will persist as long as the colonization remains and will slowly disappear (within 6 to 24 months) after H. pylori eradication. Self-ingestion experiments by Marshall and Morris showed that H. pylori colonization in the human stomach induces inflammation of the gastric mucosa, thus leading to gastritis.  Inflammation occurs in both the antrum and corpus with neutrophilic and mononuclear cells.

Gastritis can be detected in both acute and chronic phases. Acute gastritis is less commonly detected since it is normally asymptomatic. In some patients with acute gastritis, normally those who have either “deliberately or inadvertently ingested H. pylori or underwent procedures with contaminated material” may cause gastrointestinal upset for a period of months and then will suddenly resolve itself.  Most cases of acute gastritis, however, do not resolve on their own.

A 2004 set of controlled studies of acute gastritis (caused by deliberate infection of healthy volunteers with H. pylori), showed this phase tends be associated considerable inflammation of both the proximal and distal stomach mucosa, as well as hypochlorihydria. The bacterium imbeds itself in the mucous layer of the gastric mucosa and releases large amounts of urease, in order to breakdown urea to alkaline ammonia and carbon dioxide. This neutralizes the gastric acid in the immediate area and conveys a bubble of protection for the H. pylori.

The pathogen further protects itself by creating an inflammatory cascade. As this cascade progresses acute gastritis can slowly progress to a more chronic condition.^[5] Once the infection has reached a chronic level, T- and B-cell lymphocytes will be present and be followed by infiltration of numerous polymorphonuclear leukocytes cells in the lamina propria and gastric epithelium. These leukocytes will eventually phagocytize the bacteria and their presence is a key diagnostic detector of active gastritis.

The inflammatory cascade process begins with the attachment of H pylori with the surface mucosa. This results in the release of the pro-inflammatory cytokine, interleukin (IL)-8, and leads to activation of polymorphonuclear cells. High levels of cytokines, particularly tumor necrosis factor-a (TNF-α)5 and multiple interleukins (e.g., IL-6, IL-8, IL-10), are detected in the gastric mucosa of patients with H pylori gastritis. Leukotriene levels, especially Leukotriene B4 will also be elevated.

This inflammatory response leads to functional changes in the stomach. For example, according to Kusters report in the 2006 Clinical Microbiology Review, research has show there to be a close correlation between acid secretion levels and the distribution of the gastritis. A  2006 article published in the Clinical Microbiology Review by Holly Scott Algood and Timothy L. Cover showed that by releasing Leukotriene B4, which is cytotoxic to gastric epithelium, parietal cells are inhibited, leading to reduced acid secretion. The cycle continues in this manner, continued inflammation, continued loss of parietal cells, continued acid secretion allow the bacterium to further colonize.