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NOS-2 Inhibition in Phosgene-Induced Acute Lung Injury.

Piotr T Filipczak1, Albert P Senft2, JeanClare Seagrave2

  • 1*Environmental Respiratory Health and Chemistry and Inhalation Exposure Programs, Lovelace Respiratory Research Institute, Albuquerque, New Mexico 87108 and Department of Medicine, Division of Pulmonary and Critical Care Medicine, Brigham & Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115 *Environmental Respiratory Health and Chemistry and Inhalation Exposure Programs, Lovelace Respiratory Research Institute, Albuquerque, New Mexico 87108 and Department of Medicine, Division of Pulmonary and Critical Care Medicine, Brigham & Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115.

Toxicological Sciences : an Official Journal of the Society of Toxicology
|April 15, 2015
PubMed
Summary

Inhaled nitric oxide synthase 2 (NOS-2) inhibitors protect against phosgene-induced lung injury by preserving epithelial barrier integrity and surfactant protein B (SP-B) expression.

Keywords:
acute lung injurylung epitheliumnitric oxide synthase 2phosgenesurfactant protein Btight junction protein 1

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Area of Science:

  • Toxicology
  • Pulmonary Medicine
  • Biochemistry

Background:

  • Phosgene exposure causes severe acute lung injury (ALI) with high mortality, lacking targeted treatments.
  • Nitric oxide synthase 2 (NOS-2) is upregulated post-phosgene exposure, but its role in ALI pathogenesis is unclear.
  • Previous research linked NOS-2 to exacerbated ALI via surfactant protein B (SP-B) downregulation.

Purpose of the Study:

  • To investigate the role of NOS-2 in phosgene-induced ALI.
  • To test the hypothesis that inhaled selective NOS-2 inhibition mitigates phosgene-induced ALI.

Main Methods:

  • Mice were exposed to inhaled phosgene.
  • A selective NOS-2 inhibitor (1400 W) was administered via inhalation or systemically.
  • Lung injury, epithelial barrier integrity, SP-B, and tight junction protein zonula occludens 1 (ZO-1) expression were assessed.
  • Transcriptional regulation of ZO-1 by NOS-2 was studied in human lung epithelial cells.

Main Results:

  • Inhaled phosgene increased lung injury markers and NOS-2 expression.
  • Inhaled 1400 W significantly attenuated phosgene-induced ALI and preserved epithelial barrier integrity.
  • Aerosolized 1400 W increased SP-B and prevented ZO-1 downregulation.
  • NOS-2-derived nitric oxide transcriptionally downregulated ZO-1 in human lung cells.

Conclusions:

  • Lung NOS-2 plays a critical role in phosgene-induced ALI development.
  • Inhaled NOS-2 inhibitors represent a promising therapeutic strategy for phosgene-induced ALI.
  • Targeting NOS-2-mediated ZO-1 downregulation offers a novel approach to ameliorate ALI vascular leak.