Abstract

Active soluble Fas ligand (sFasL) accumulates in lung fluid of patients with acute respiratory distress syndrome (ARDS), and causes apoptosis and inflammation in lung epithelial cells [1]. Alveolar epithelial damage induced by Fas receptor activation results in protein-rich lung edema [2]. Dysfunction of the tight junction proteins may contribute to the formation of lung edema.

Highlights

  • Active soluble Fas ligand accumulates in lung fluid of patients with acute respiratory distress syndrome (ARDS), and causes apoptosis and inflammation in lung epithelial cells [1]

  • Alveolar epithelial damage induced by Fas receptor activation results in protein-rich lung edema [2]

  • Dysfunction of the tight junction proteins may contribute to the formation of lung edema

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Summary

Objectives

Determine whether sFasL increases protein permeability of the alveolar epithelium by mechanisms involving disruption of the tight junction proteins in ARDS.

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