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Published ahead of print on March 16, 2006, doi:10.1165/rcmb.2005-0241OC

Am. J. Respir. Cell Mol. Biol., Volume 35, Number 2, August 2006, 227-235

A more recent version of this article appeared on August 1, 2006
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Submitted on July 1, 2005
Revised on March 16, 2006

Resident Alveolar Macrophages are Replaced by Recruited Monocytes in Response to Endotoxin-induced Lung Inflammation

Ulrich A Maus1*, Simeon Janzen2, Gerhard Wall2, Mrigank Srivastava1, Timothy S Blackwell3, John W Christman4, Werner Seeger2, Tobias Welte5, and Juergen Lohmeyer2

1 Department of Internal Medicine, Division of Pulmonary and Critical Care Medicine, University Giessen Lung Center (UGLC), Giessen, Germany; Department of Pulmonary Medicine, Hannover School of Medicine, Hannover, Germany, 2 Department of Internal Medicine, Division of Pulmonary and Critical Care Medicine, University Giessen Lung Center (UGLC), Giessen, Germany, 3 Department of Medicine, Division of Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University School of Medicine, Nashville, TN, USA, 4 Section of Pulmonary, Critical Care, and Sleep Medicine, University of Illinois at Chicago, Chicago, IL, USA, 5 Department of Pulmonary Medicine, Hannover School of Medicine, Hannover, Germany

* To whom correspondence should be addressed. E-mail: Maus.Ulrich{at}mh-hannover.de.

In the acute respiratory distress syndrome, recruited peripheral blood monocytes results in expansion of the total pool of resident alveolar macrophages. The fate of resident macrophages or whether recruited monocytes are selectively eliminated from the alveolar air space or differentiate into resident alveolar macrophages during the resolving phase of inflammation has not been determined. Here, we analyzed the kinetics of resident and recruited macrophage turnover within the alveolar air space of untreated and LPS-challenged mice. Using bone marrow chimeric CD45.2 mice that were generated by lethal irradiation of CD45.2 alloantigen-expressing recipient mice and bone marrow transplantation from CD45.1 alloantigen-expressing donor mice, we employed a flow cytometric approach to distinguish recipient from donor-type macrophages in bronchoalveolar lavage fluids. Our data show that resident alveolar macrophages of untreated chimeric CD45.2 mice are very slowly replaced by constitutively immigrating CD45.1 positive monocytes, resulting in a replacement rate of approximately 40% by one year. In contrast, more than 85% of the resident CD45.2 positive alveolar and lung homogenate macrophages were exchanged by donor CD45.1 expressing macrophages within 2 months following treatment with E. coli endotoxin (LPS). Importantly, FACS analysis of increased annexin V binding to both recipient and donor-type macrophages revealed increased apoptotic events to underly this endotoxin-driven inflammatory macrophage turnover. Collectively, the data show that under baseline conditions the alveolar macrophage turnover exhibits very slow kinetics, whereas acute lung inflammation in response to treatment with LPS triggers a brisk acceleration of recruitment of monocytes that replace the resident alveolar macrophage population.




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