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Ann Thorac Surg 2008;86:1774-1779. doi:10.1016/j.athoracsur.2008.07.071
© 2008 The Society of Thoracic Surgeons
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Original Articles: General Thoracic

Alveolar Macrophage Secretory Products Effect Type 2 Pneumocytes Undergoing Hypoxia-Reoxygenation

Anton S. McCourtie, MRCS, Alexander S. Farivar, MD, Steven M. Woolley, MRCS, Heather E. Merry, MD, Patrick S. Wolf, MD, Brendan Mackinnon-Patterson, BS, John C. Keech, MD, Elizabeth FitzSullivan, MD, Michael S. Mulligan, MD*

Department of Surgery, Division of Cardiothoracic Surgery, University of Washington Medical Center, Seattle, Washington

Accepted for publication July 24, 2008.

* Address correspondence to Dr Mulligan, University of Washington Medical Center, Box 356310, Seattle, WA 98195 (Email: msmmd{at}u.washington.edu).

Background: Activation of the alveolar macrophage is centrally important to the development of lung ischemia reperfusion injury. Alveolar macrophages and type 2 pneumocytes secrete a variety of proinflammatory mediators in response to oxidative stress. The manner in which they interact and how the macrophage may influence pneumocyte responses in lung ischemia reperfusion injury is unknown. Utilizing an in vitro model of hypoxia and reoxygenation, we sought to determine if the proinflammatory response of type 2 pneumocytes to oxidative stress would be amplified by alveolar macrophage secretory products.

Methods: Cultured pneumocytes were exposed to control media or media from cultured macrophages exposed to hypoxia and reoxygenation. Pneumocytes were subsequently subjected to hypoxia and reoxygenation and assessed for both nuclear translocation of nuclear factor kappa B and inflammatory cytokine and chemokine secretion. To examine for any reciprocal interactions, we reversed the experiment, exposing macrophages to conditioned pneumocyte media.

Results: In the presence of media from stimulated macrophages, production of proinflammatory mediators by type 2 pneumocytes was dramatically enhanced. In contrast, exposure of the macrophage to conditioned pneumocyte media had an inhibitory effect on macrophage responses subsequently exposed to hypoxia and reoxygenation.

Conclusions: The alveolar macrophage drives the development of lung reperfusion injury in part through amplification of the inflammatory response of type 2 pneumocytes subjected to hypoxia and reoxygenation.


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Invited Commentary
Niels P. van der Kaaij and Ad J.J.C. Bogers
Ann. Thorac. Surg. 2008 86: 1779-1780. [Extract] [Full Text] [PDF]



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 Ann. Thorac. Surg.Home page
N. P. van der Kaaij and A. J.J.C. Bogers
Invited Commentary
Ann. Thorac. Surg., December 1, 2008; 86(6): 1779 - 1780.
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