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Barrett's esophagus is a medical condition where the esophageal mucosa is significantly damaged by stomach acid or other digestive fluids, often due to long-term exposure associated with gastroesophageal reflux disease (GERD). In GERD, a weakened or abnormally relaxed lower esophageal sphincter allows stomach acid to flow persistently into the esophagus.
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Esophageal strictures involve abnormal narrowing or tightening of the esophagus. They vary in length and severity, ranging from mild constriction to complete obstruction, and are classified as benign (noncancerous) or malignant (cancerous).
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Individuals with Barrett's esophagus are often asymptomatic, but they may experience symptoms commonly associated with GERD, such as heartburn and acid regurgitation. Additional symptoms can include difficulty swallowing, chest pain, unintentional weight loss, blood in the stool (which may appear black, tarry, or bloody), and episodes of vomiting.
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The esophagus, a muscular conduit linking the pharynx and stomach, measures roughly 10 inches (25.4 cm) and sits behind the trachea. It remains collapsed when not swallowing. The esophagus follows a predominantly straight path through the thoracic mediastinum and enters the abdominal cavity through a diaphragmatic opening known as the esophageal hiatus.
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Characterizing caspase-1 involvement during esophageal disease progression.

Gillian Barber1,2, Akanksha Anand3, Katarzyna Oficjalska1

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Cancer Immunology, Immunotherapy : CII
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Caspase-1 is elevated in Barrett's esophagus (BE), a precancerous condition. Inhibiting caspase-1 reduced inflammatory markers, suggesting it's a potential therapeutic target for preventing esophageal adenocarcinoma (EAC) progression.

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Area of Science:

  • Gastroenterology
  • Inflammation research
  • Cancer biology

Background:

  • Barrett's esophagus (BE) is a precancerous condition linked to chronic inflammation.
  • Inflammasome signaling, including caspase-1 activation, drives inflammation and cell death.
  • Caspase-1 plays a role in secreting inflammatory cytokines like IL-1β and IL-18.

Purpose of the Study:

  • To investigate caspase-1 expression and its functional role in the progression from normal esophagus to BE and esophageal adenocarcinoma (EAC).
  • To assess the impact of caspase-1 inhibition on inflammatory mediator secretion in BE models.

Main Methods:

  • Utilized three models: human esophageal cell lines, a murine BE model, and patient-derived tissues.
  • Analyzed caspase-1 expression in epithelial and stromal compartments.
  • Cultured BE patient biopsies and murine BE organoids ex vivo with a caspase-1 inhibitor to measure cytokine and chemokine secretion.

Main Results:

  • Epithelial caspase-1 expression was significantly increased in BE.
  • Stromal caspase-1 levels correlated with inflammation severity.
  • Caspase-1 inhibition in BE organoids reduced IL-1β and CXCL1 secretion.

Conclusions:

  • Caspase-1 activity is enhanced in BE and contributes to the secretion of inflammatory mediators.
  • Targeting caspase-1 may represent a novel therapeutic strategy to prevent progression from BE to EAC.