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Automated Measurement of Pulmonary Emphysema and Small Airway Remodeling in Cigarette Smoke-exposed Mice
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Receptor for advanced glycation endproducts (RAGE) maintains pulmonary structure and regulates the response to

Lisa Wolf1, Christian Herr1, Julia Niederstraßer1

  • 1Department of Internal Medicine V - Pulmonology, Allergology and Critical Care Medicine, Saarland University, Homburg, Germany.

Plos One
|July 6, 2017
PubMed

Insights

The receptor for advanced glycation endproducts (RAGE) is crucial for lung structure and function. RAGE deficiency impairs alveolar epithelial cell differentiation and alters inflammatory responses, impacting lung health.

Area of Science:

  • Pulmonary medicine
  • Cell biology
  • Immunology

Background:

  • The receptor for advanced glycation endproducts (RAGE) is highly expressed in the lung, but its precise physiological roles remain unclear.
  • Understanding RAGE's function is critical for addressing lung diseases.

Purpose of the Study:

  • To investigate the contribution of RAGE to the physiological functions and structural integrity of the lung.
  • To elucidate RAGE's role in alveolar epithelial cell differentiation and inflammatory responses in the lung.

Main Methods:

  • Comparative analysis of pulmonary mechanics and lung structure in wildtype and RAGE-deficient (RAGE-/-) mice.
  • In vitro studies using primary murine alveolar epithelial cells and RAGE-deficient alveolar macrophages stimulated with Toll-like receptor (TLR) ligands.
  • Assessment of inflammatory responses following acute and chronic cigarette smoke exposure.

Main Results:

  • RAGE deficiency led to spontaneous loss of lung structure, characterized by increased mean chord length and respiratory system compliance, and decreased elastance.
  • Alveolar epithelial cells from RAGE-/- mice exhibited altered differentiation and defective barrier formation in vitro.
  • RAGE-deficient macrophages showed reduced release of pro-inflammatory cytokines and chemokines upon TLR ligand stimulation.
  • RAGE deficiency modified the inflammatory response to acute cigarette smoke, with increased macrophage influx and decreased keratinocyte-derived chemokine (KC) release.
  • RAGE-/- mice did not exhibit emphysema-like changes upon chronic cigarette smoke exposure.

Conclusions:

  • RAGE is essential for maintaining normal pulmonary structure and alveolar epithelial cell differentiation.
  • RAGE plays a significant role in mediating inflammatory responses within the lung, particularly in the context of cigarette smoke exposure.
  • Targeting RAGE may offer therapeutic potential for managing lung inflammation and associated pathologies.

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