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What lurks beneath: IL-11, via Stat3, promotes inflammation-associated gastric tumorigenesis

Juanita L Merchant1

  • 1Department of Internal Medicine, University of Michigan, 109 Zina Pitcher Place, BSRB Room 2051, Ann Arbor, Michigan 48198-2200, USA. merchanj@umich.edu

The Journal of Clinical Investigation
|April 24, 2008
PubMed

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Gastritis II: Pathophysiology

The pathophysiology of gastritis begins with the colonization of the stomach lining by Helicobacter pylori (H. pylori). This bacterium spreads mainly via the oral-oral route through saliva or shared utensils, and can also be transmitted in overcrowded or unhygienic environments through contaminated water, despite its brief survival outside the body.ColonizationOnce ingested, H. pylori enters the stomach and begins colonization by navigating through the mucus layer lining the stomach wall. It...
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Gastritis-II: Pathophysiology

Gastritis is marked by disruption of the mucosal barrier that usually protects the stomach tissue from digestive juices and manifests in acute and chronic forms.
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
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Inflammatory Bowel Disease III: Crohn's Disease

Crohn’s disease is a chronic, relapsing form of inflammatory bowel disease characterized by segmental, transmural inflammation that can affect any part of the gastrointestinal tract. Its pathogenesis arises from a combination of genetic susceptibility, environmental exposures, epithelial barrier dysfunction, and immune dysregulation. Together, these factors lead to an exaggerated immune response against components of the gut microbiome.Genetic and Environmental InfluencesMultiple genetic...
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The clinical manifestations of gastritis can vary depending on the cause and type of gastritis, but some common symptoms may include the following.
Clinical manifestations of acute gastritis
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