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Published ahead of print on January 13, 2006, doi:10.1164/rccm.200509-1518OC

Am. J. Respir. Crit. Care Med., Volume 173, Number 7, April 2006, 781-792

A more recent version of this article appeared on April 1, 2006
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Submitted on September 28, 2005
Accepted on January 9, 2006

A Vicious Circle of Alveolar Macrophages and Fibroblasts Perpetuates Pulmonary Fibrosis via CCL18

Antje Prasse1*, Dmitri V Pechkovsky1, Galen B Toews2, Wolfgang Jungraithmayr3, Florian Kollert1, Torsten Goldmann4, Ekkehard Vollmer4, Joachim Muller-Quernheim1, and Gernot Zissel1

1 Department of Pneumology, Medical Center, University Hospital Freiburg, Freiburg, Germany, 2 Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, Michigan, USA, 3 Department of Thoracic Surgery, University Hospital Freiburg, Freiburg, Germany, 4 Division of Clinical and Experimental Pathology, Research Center Borstel, Borstel, Germany

* To whom correspondence should be addressed. E-mail: prasse{at}medizin.ukl.uni-freiburg.de.

Rationale: Recently, models of macrophage activation have been revised. Macrophages stimulated with TH2-cytokines have been classified as alternatively activated. Objectives: This study examines the expression and regulation of CC chemokine ligand 18 (CCL18), a marker of alternative activation, by human alveolar macrophages (AM). Methods: AM obtained from bronchoalveolar lavage (BAL) of patients with idiopathic pulmonary fibrosis, sarcoidosis, hypersensitivity pneumonitis (n=69) and healthy volunteers (n=22). Expression of CCL18 was determined by quantitative RT-PCR, in situ hybridization, flow cytometry, and immunohistochemistry respectively. Measurements and Main Results: Spontaneous CCL18 production by BAL-cells was markedly increased in patients with pulmonary fibrosis and correlated negatively with pulmonary function test parameters. CCL18 gene expression and protein production were up-regulated in normal AM following TH2-cytokine stimulation and/or co-culture with human lung fibroblasts. Native collagen significantly up-regulated CCL18 expression in normal AM activated with TH2 cytokines via a mechanism mediated by {beta}2-integrin/ scavenger receptor(s). Furthermore culture supernatants of AM from patients with IPF increased collagen production by normal lung fibroblasts partly mediated via CCL18. Conclusions: Our findings suggest that alveolar macrophages from patients with pulmonary fibrosis disclose a phenotype of alternative activation and might be a part of a positive feedback loop with lung fibroblasts perpetuating fibrotic processes.
Key words: IPF, pulmonary fibrosis, CCL18, collagen, alveolar macrophages




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