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Alveolar macrophage secretory products effect type 2 pneumocytes undergoing hypoxia-reoxygenation

Anton S McCourtie1, Alexander S Farivar, Steven M Woolley

  • 1Department of Surgery, Division of Cardiothoracic Surgery, University of Washington Medical Center, Seattle, Washington, USA.

The Annals of Thoracic Surgery
|November 22, 2008
PubMed
Abstract

Insights

Alveolar macrophages amplify type 2 pneumocyte inflammation during lung ischemia reperfusion injury. Macrophage products enhance pneumocyte response to oxidative stress, driving injury development.

Area of Science:

  • Pulmonary Medicine
  • Immunology
  • Cell Biology

Background:

  • Alveolar macrophage activation is critical in lung ischemia reperfusion injury (IRI).
  • Macrophages and type 2 pneumocytes release inflammatory mediators under oxidative stress.
  • The interaction between these cells in lung IRI is not well understood.

Purpose of the Study:

  • To investigate if alveolar macrophage secretory products amplify type 2 pneumocyte inflammatory responses to oxidative stress in an in vitro lung IRI model.

Main Methods:

  • Type 2 pneumocytes were exposed to media from hypoxia/reoxygenation-stimulated macrophages.
  • Pneumocyte nuclear factor-kappa B translocation and cytokine/chemokine secretion were assessed.
  • Reciprocal experiments exposed macrophages to conditioned pneumocyte media.

Main Results:

  • Media from stimulated macrophages significantly enhanced proinflammatory mediator production by type 2 pneumocytes.
  • Exposure to conditioned pneumocyte media inhibited subsequent macrophage inflammatory responses.

Conclusions:

  • Alveolar macrophages play a key role in lung IRI by amplifying type 2 pneumocyte inflammatory responses.
  • This amplification occurs in response to hypoxia and reoxygenation.

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