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Investigating Intestinal Barrier Breakdown in Living Organoids
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STING-mediated intestinal barrier dysfunction contributes to lethal sepsis.

Qiongyuan Hu1, Huajian Ren2, Guanwei Li3

  • 1Research Institute of General Surgery, Jinling Hospital, Medical School of Nanjing University, Nanjing, China; Medical School of Nanjing University, Nanjing, China.

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Summary
This summary is machine-generated.

The stimulator of interferons genes (STING) pathway exacerbates sepsis by damaging the gut barrier and increasing cell death. Inhibiting this pathway may protect against sepsis-induced intestinal damage.

Keywords:
IEC apoptosisIntestinal inflammationSTINGSepsis

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Area of Science:

  • Immunology
  • Gastroenterology
  • Sepsis Pathophysiology

Background:

  • Abdominal sepsis compromises gut integrity, increasing cell apoptosis and barrier permeability.
  • Intestinal epithelial cells (IECs) form a critical barrier and are involved in mucosal immune responses.
  • The stimulator of interferons genes (STING) pathway is implicated in uncontrolled inflammation and gut immunity.

Purpose of the Study:

  • To investigate the role of STING signaling in sepsis and intestinal barrier function.
  • To examine STING expression in human and mouse models of abdominal sepsis.
  • To explore therapeutic strategies targeting the STING pathway.

Main Methods:

  • Analysis of intestinal biopsies and peripheral blood mononuclear cells from human septic patients.
  • Utilizing a mouse model of abdominal sepsis induced by cecal ligation perforation (CLP).
  • Comparing STING knockout mice and wild-type mice, and administering a STING agonist (DMXAA).
  • Investigating the role of mitochondrial DNA (mtDNA) and DNase I administration.

Main Results:

  • Elevated STING expression in human septic patients correlated with intestinal inflammation and enterocyte damage.
  • STING signaling was activated in mice post-CLP.
  • STING knockout mice exhibited reduced inflammation, permeability, and bacterial translocation.
  • STING activation exacerbated apoptosis and inflammation in septic mice.
  • Mitochondrial DNA (mtDNA) release activated STING, contributing to inflammation.
  • DNase I treatment reduced inflammatory markers, organ damage, and bacterial translocation.

Conclusions:

  • The STING signaling pathway promotes IEC apoptosis and disrupts the intestinal barrier in sepsis.
  • Targeting the mtDNA-STING pathway offers a potential therapeutic strategy for sepsis-induced intestinal dysfunction.
  • This pathway regulation may promote mucosal healing and protect the intestinal barrier in septic patients.