title: Gastroduodenal mucosal defense.
abstract: OBJECTIVE
  The gastroduodenum has multiple means by which it resists injury from intrinsic and extrinsic factors, including gastric acid, nonsteroidal anti-inflammatory drugs, and Helicobacter pylori. We review recent insights into the mechanisms by which the gastroduodenum resists injury and discuss factors contributing to defensive failure.
  
  
  RESULTS
  Duodenal bicarbonate secretion, a primary defensive mechanism, is mediated by the downregulated in adenoma anion exchanger and is stimulated by estrogens. Nonsteroidal anti-inflammatory drug gastric damage is dependent on toll-like receptor signaling. Portal hypertensive gastropathy impairs extracellular signal-regulated kinase 1/2 phosphorylation, increasing oxidative stress. H. pylori-induced peptic ulcer disease is associated with inadequate regulatory T cell responses.
  
  
  CONCLUSIONS
  Enhanced understanding of the mechanisms of gastroduodenal defense and injury provides new insight into potential therapeutic targets, which contributes towards the development of more well tolerated and more effective therapies.
authors: aDepartment of Internal Medicine, UCLA Medical Center, USA bGreater Los Angeles Veteran Affairs Healthcare System, WLAVA Medical Center, Los Angeles, California, USA.
authors: Hamed
authors: H
authors: Nayeb-Hashemi
authors: Jonathan D
authors: JD
authors: Kaunitz
mesh_terms: D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects; D001241:Aspirin / Q000009:adverse effects; D001639:Bicarbonates / Q000378:metabolism*; D004386:Duodenum / Q000276:immunology* / Q000378:metabolism; D005753:Gastric Mucosa / Q000187:drug effects / Q000276:immunology* / Q000378:metabolism; D015658:HIV Infections / Q000276:immunology; D016481:Helicobacter Infections / Q000276:immunology; D016480:Helicobacter pylori; D006801:Humans; D006975:Hypertension, Portal / Q000276:immunology*; D018928:Immunity, Mucosal / Q000502:physiology*; D000070116:Lotus / Q000378:metabolism; D009077:Mucins / Q000378:metabolism; D009479:Neuropeptides / Q000502:physiology; D018384:Oxidative Stress; D010437:Peptic Ulcer / Q000139:chemically induced* / Q000276:immunology; D010766:Phosphorylation; D013601:T-Lymphocytes / Q000276:immunology; D042461:Vascular Endothelial Growth Factor A / Q000502:physiology
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D001639:Bicarbonates; D009077:Mucins; D009479:Neuropeptides; D042461:Vascular Endothelial Growth Factor A; D001241:Aspirin