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Ann Thorac Surg 2008;86:1779-1780. doi:10.1016/j.athoracsur.2008.09.021
© 2008 The Society of Thoracic Surgeons
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Original Articles: General Thoracic

Invited Commentary

Niels P. van der Kaaij, MD, Ad J.J.C. Bogers, MD, PhD

Department of Cardiothoracic Surgery, Erasmus MC, Dr. Molewaterplein 50, Rotterdam, 3015 GE, the Netherlands

(Email: npvdkaaij@gmail.com; a.j.j.c.bogers@erasmusmc.nl).

The first 20% of the full text of this article appears below.

The study by McCourtie and colleagues [1] investigates whether the inflammatory response of type 2 pneumocytes (T2P) to oxidative stress is influenced by mediators produced by alveolar macrophages (AMs) exposed to hypoxia and reoxygenation (HR) or the other way around. The authors demonstrate by use of an in-vitro cell culture model that production of pro-inflammatory mediators by T2P was increased after incubation with media from HR-stimulated AMs. Incubating AMs with T2P media exposed to HR resulted in inhibition of cytokine production. The methodology of this article closely resembles an earlier report by this group, which showed that mediators produced by AMs . . . [Full Text of this Article]


Related Article

Alveolar Macrophage Secretory Products Effect Type 2 Pneumocytes Undergoing Hypoxia-Reoxygenation
Anton S. McCourtie, Alexander S. Farivar, Steven M. Woolley, Heather E. Merry, Patrick S. Wolf, Brendan Mackinnon-Patterson, John C. Keech, Elizabeth FitzSullivan, and Michael S. Mulligan
Ann. Thorac. Surg. 2008 86: 1774-1779. [Abstract] [Full Text] [PDF]





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