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Articles in PresS, published online ahead of print January 18, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00453.2001
Submitted on November 26, 2001
Accepted on January 10, 2002
1 Internal Medicine, Justus-Liebig-University, Giessen, Germany
2 Department of Medicine, Division of Allergy, Pulmonary and Critical Care Medicine, and Department of Veterans Affairs, Vanderbilt University School of Medicine, Nashville, TN, USA
3 Medical Policlinic, University of Munich, Munich, Germany
* To whom correspondence should be addressed. E-mail: Ulrich.A.Maus{at}med.uni-giessen.de.
Intratracheal instillation of the monocyte chemoattractant JE/MCP-1 in mice was recently shown to cause increased alveolar monocyte accumulation in the absence of lung inflammation, whereas combined JE/MCP-1/LPS challenge provoked acute lung inflammation with successive waves of early alveolar neutrophil and delayed alveolar monocyte influx. We now evaluated the role of resident alveolar macrophages (rAM) in these leukocyte recruitment events and related phenomena of lung inflammation. Depletion of rAM by pre-treatment of mice with liposome-encapsulated dichloromethylene-diphosphonate (clodronate) did not affect the sole JE/MCP-1 driven alveolar monocyte accumulation, despite the observation that rAM constitutively expressed the JE/MCP-1 receptor, CCR2, as analyzed by flow cytometry and immunohistochemistry. In contrast, depletion of rAM largely suppressed alveolar cytokine release (TNF-
, MIP-2) as well as alveolar neutrophil and monocyte recruitment profiles following combined JE/MCP-1/LPS treatment. Despite this strongly attenuated alveolar inflammatory response, increased lung vascular permeability with alveolar protein leakage was still observed in the rAM-depleted mice undergoing JE/MCP-1 plus LPS challenge. This leakage response was abrogated by co-depletion of circulating neutrophils or intravenous administration of anti-CD18 mAb. Collectively, rAM are not involved in JE/MCP-1-driven alveolar monocyte recruitment in non-inflamed lungs, but largely contribute to the alveolar cytokine response and the enhanced early neutrophil and delayed monocyte influx under inflammatory conditions (JE/MCP-1 plus LPS deposition). Loss of lung barrier function observed under these conditions is rAM-independent, but involves circulating neutrophils via ß2 integrin engagement.
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