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Nitric oxide directly impairs intestinal barrier function.

Da-Zhong Xu1, Qi Lu, Edwin A Deitch

  • 1Department of Surgery, UMDNJ-New Jersey Medical School, Newark 07103-2714, USA.

Shock (Augusta, Ga.)
|February 12, 2002
PubMed
Summary
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Excess nitric oxide (NO) directly damages gut barrier function, increasing bacterial translocation and cell death. This study shows NO production is linked to endotoxin- and cytokine-induced gut barrier dysfunction.

Area of Science:

  • Gastroenterology
  • Immunology
  • Cell Biology

Background:

  • Excess nitric oxide (NO) is linked to impaired gut barrier function in endotoxin-induced conditions.
  • Enterocyte-derived NO may contribute to gut barrier dysfunction.

Purpose of the Study:

  • To investigate the direct effects of NO on intestinal mucosal barrier function ex vivo.
  • To determine the role of NO production in endotoxin- and cytokine-induced barrier dysfunction in enterocytes.

Main Methods:

  • Ex vivo Ussing chamber experiments with ileal membranes and IEC-6 enterocyte monolayers exposed to NO donor SNAP.
  • Measurement of bacterial translocation (BT), phenol red permeability, histology, and cell death.
  • Assessment of NO production, inducible nitric oxide synthase (iNOS) mRNA levels, and monolayer permeability in enterocytes exposed to lipopolysaccharide or cytokine mixtures.

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Main Results:

  • High concentrations of SNAP (1-2 mM) increased BT and permeability in ileal membranes and enterocyte monolayers.
  • SNAP exposure led to mucosal injury, decreased electrical resistance, and increased cell death.
  • Endotoxin and cytokine mixtures increased NO production, iNOS mRNA expression, and monolayer permeability in enterocytes.

Conclusions:

  • Nitric oxide directly impairs intestinal mucosal and enterocyte monolayer barrier function.
  • Increased NO production and iNOS expression are associated with endotoxin- and cytokine-induced gut barrier dysfunction.