Alveolar-Capillary Membrane-Related Pulmonary Cells as a Target in Endotoxin-Induced Acute Lung Injury

Int J Mol Sci. 2019 Feb 15;20(4):831. doi: 10.3390/ijms20040831.

Abstract

The main function of the lungs is oxygen transport from the atmosphere into the blood circulation, while it is necessary to keep the pulmonary tissue relatively free of pathogens. This is a difficult task because the respiratory system is constantly exposed to harmful substances entering the lungs by inhalation or via the blood stream. Individual types of lung cells are equipped with the mechanisms that maintain pulmonary homeostasis. Because of the clinical significance of acute respiratory distress syndrome (ARDS) the article refers to the physiological role of alveolar epithelial cells type I and II, endothelial cells, alveolar macrophages, and fibroblasts. However, all these cells can be damaged by lipopolysaccharide (LPS) which can reach the airspaces as the major component of the outer membrane of Gram-negative bacteria, and lead to local and systemic inflammation and toxicity. We also highlight a negative effect of LPS on lung cells related to alveolar-capillary barrier and their response to LPS exposure. Additionally, we describe the molecular mechanism of LPS signal transduction pathway in lung cells.

Keywords: acute respiratory distress syndrome; alveolar epithelial cells; alveolar macrophages; bacterial lipopolysaccharide; endothelial cells; fibroblasts.

Publication types

  • Review

MeSH terms

  • Acute Lung Injury / chemically induced
  • Acute Lung Injury / metabolism*
  • Acute Lung Injury / pathology
  • Alveolar Epithelial Cells / drug effects*
  • Alveolar Epithelial Cells / metabolism
  • Alveolar Epithelial Cells / pathology
  • Capillaries / drug effects
  • Capillaries / pathology
  • Cell Membrane / drug effects
  • Cell Membrane / metabolism
  • Humans
  • Lipopolysaccharides / toxicity*
  • Lung / drug effects
  • Lung / metabolism
  • Lung / pathology
  • Oxygen / metabolism
  • Pulmonary Alveoli / drug effects
  • Pulmonary Alveoli / pathology
  • Respiratory Distress Syndrome / chemically induced
  • Respiratory Distress Syndrome / metabolism*
  • Respiratory Distress Syndrome / pathology
  • Signal Transduction / genetics

Substances

  • Lipopolysaccharides
  • Oxygen