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Cytokine-Induced Barrier Dysfunction and Lipid Signaling in a Gut-On-Chip Model.

Moran Morelli1, Mariyana V Savova2, Karla Queiroz1

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This study shows how inflammatory cytokines disrupt the gut barrier, altering lipid signaling. Medium composition significantly impacts these inflammatory responses in a gut-on-chip model.

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Area of Science:

  • Gastroenterology
  • Cell Biology
  • Biochemistry

Background:

  • The intestinal epithelial barrier is vital for gut health and homeostasis.
  • Dysfunction of this barrier is implicated in inflammatory bowel disease (IBD).
  • The role of lipid signaling in cytokine-induced barrier disruption is not well understood.

Purpose of the Study:

  • To investigate the impact of inflammatory cytokines on intestinal epithelial barrier function.
  • To explore the role of lipid signaling in cytokine-mediated barrier disruption.
  • To analyze the influence of medium composition on inflammatory responses and lipid profiles in a gut-on-chip model.

Main Methods:

  • Utilized a microfluidic gut-on-chip model with cultured epithelial tubules.
  • Exposed the luminal side to TNF-α, IL-1β, and IFN-γ under varying medium conditions.
  • Assessed barrier function using transepithelial electrical resistance (TEER), DRAQ7 staining, and actin analysis.
  • Performed lipid mediator profiling via liquid chromatography-tandem mass spectrometry.

Main Results:

  • Cytokine exposure significantly reduced TEER, indicating impaired barrier integrity.
  • Cell damage and actin remodeling were observed, with reduced effects in serum-free medium.
  • Lipid profiling revealed increased prostaglandins (e.g., PGF1α, PGE1, PGE2, PGD2) in the luminal compartment, especially under serum-free conditions.
  • Distinct eicosanoid changes, excluding prostaglandins, were noted in the basolateral compartment under serum-free conditions.

Conclusions:

  • Medium composition critically influences inflammatory responses and lipid signaling in the gut-on-chip model.
  • The study highlights the complex spatial organization of lipid mediators during inflammation-induced barrier dysfunction.
  • Provides a framework for studying the interplay of inflammation, barrier integrity, and lipid metabolism in intestinal diseases.