What is the role of H pylori in the pathogenesis of chronic gastritis?

Updated: Jun 07, 2019
  • Author: Akiva J Marcus, MD, PhD; Chief Editor: BS Anand, MD  more...
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Helicobacter pylori is the leading cause of chronic gastritis, peptic ulcer disease, gastric adenocarcinoma and primary gastric lymphoma. [7, 8, 9] First described by Marshall and Warren in 1983, H pylori is a spiral gram-negative rod that has the ability to colonize and infect the stomach; the lipopolysaccharides on the outer membrane of H pylori are a major component of its ability for colonization and persistence. [9] The bacteria survive within the mucous layer that covers the gastric surface epithelium and the upper portions of the gastric foveolae. The infection is usually acquired during childhood. Once present in the stomach, the bacteria passes through the mucous layer and becomes established at the luminal surface of the stomach causing an intense inflammatory response in the underlying tissue. [2, 9, 10, 11, 12]

The presence of H pylori is associated with tissue damage and the histologic finding of both an active and a chronic gastritis. The host response to H pylori and its bacterial products is composed of T and B lymphocytes, denoting chronic gastritis, followed by infiltration of the lamina propria and gastric epithelium by polymorphonuclear leukocytes (PMNs) that eventually phagocytize the bacteria. The presence of PMNs in the gastric mucosa is diagnostic of active gastritis. [13, 14]

Interaction of H pylori with the surface mucosa results in the release of interleukin (IL)-8, which leads to the recruitment of PMNs and may begin the entire inflammatory process. Gastric epithelial cells express class II molecules, which may increase the inflammatory response by presenting H pylori antigens, leading to the activation of numerous transcription factors, including NF-kB, AP-1 and CREB-1. This in turn leads to further cytokine release and more inflammation. High levels of cytokines, particularly tumor necrosis factor-α (TNF-α) [15] and multiple interleukins (eg, IL-1β, IL-6, IL-8, IL-10, IL-12, IL-17 and IL-18), are detected in the gastric mucosa of patients with H pylori gastritis. [13, 14] Increased frequencies of IL-17a+ and interferon gamma (IFN-γ) cells have been found in the antrum, particularly in individuals with H pylori-induced gastric ulcers. [16]

Leukotriene levels are also quite elevated, especially the level of leukotriene B4, which is synthesized by the host neutrophils and is cytotoxic to the gastric epithelium. [17] This inflammatory response leads to functional changes in the stomach, depending on the areas of the stomach involved. When the inflammation affects the gastric corpus, parietal cells are inhibited, leading to reduced acid secretion. Continued inflammation results in loss of the parietal cells, and the reduction in acid secretion becomes permanent.

Antral inflammation alters the interplay between gastrin and somatostatin secretion, affecting G cells (gastrin-secreting cells) and D cells (somatostatin-secreting cells), respectively. Specifically, gastrin secretion is abnormal in individuals who are infected with H pylori, with an exaggerated meal-stimulated release of gastrin being the most prominent abnormality. [18]

When the infection is cured, neutrophil infiltration of the tissue quickly resolves, with slower resolution of the chronic inflammatory cells. Paralleling the slow resolution of the monocytic infiltrates, meal-stimulated gastrin secretion returns to normal. [19]

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