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1 Department of Internal Medicine, Division of Pneumology, 4 Division of Pathology, Justus Liebig University, 35392 Giessen; 3 Medical Policlinic, University of Munich, 81366 Munich, Germany; 2 Department of Medicine, Division of Allergy, Pulmonary, and Critical Care Medicine, Vanderbilt University School of Medicine, Nashville 37232; and Department of Veterans Affairs, Nashville, Tennessee 37212
Intratracheal instillation of
the monocyte chemoattractant JE/monocyte chemoattractant protein
(MCP)-1 in mice was recently shown to cause increased alveolar
monocyte accumulation in the absence of lung inflammation, whereas
combined JE/MCP-1/lipopolysaccharide (LPS) challenge provoked acute
lung inflammation with early alveolar neutrophil and delayed alveolar
monocyte influx. We evaluated the role of resident alveolar
macrophages (rAM) in these leukocyte recruitment events and related
phenomena of lung inflammation. Depletion of rAM by pretreatment of
mice with liposomal clodronate did not affect the 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 as well as neutrophil and
monocyte recruitment profiles upon combined JE/MCP-1/LPS treatment.
Despite this strongly attenuated alveolar inflammatory response,
increased lung permeability was still observed in rAM-depleted mice
undergoing JE/MCP-1/LPS challenge. Lung leakage was abrogated by
codepletion of circulating neutrophils or administration of anti-CD18.
Collectively, rAM are not involved in JE/MCP-1-driven alveolar monocyte
recruitment in noninflamed lungs but largely contribute to the alveolar
cytokine response and enhanced early neutrophil and delayed monocyte
influx under inflammatory conditions (JE/MCP-1/LPS deposition). Loss of
lung barrier function observed under these conditions is rAM
independent but involves circulating neutrophils via
2-integrin engagement.
monocyte; neutrophil; vascular permeability; lung; inflammation; depletion
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