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A vicious circle of alveolar macrophages and fibroblasts perpetuates pulmonary fibrosis via CCL18.
Am J Respir Crit Care Med. 2006 Apr 01; 173(7):781-92.AJ

Abstract

RATIONALE

Recently, models of macrophage activation have been revised. Macrophages stimulated with Th2 cytokines have been classified as alternatively activated.

OBJECTIVES

This article examines the expression and regulation of CC chemokine ligand 18 (CCL18), a marker of alternative activation, by human alveolar macrophages (AMs).

METHODS

AM were obtained from bronchoalveolar lavage (BAL) fluid of patients with idiopathic pulmonary fibrosis, sarcoidosis, or hypersensitivity pneumonitis (n = 69) and healthy volunteers (n = 22). Expression of CCL18 was determined by quantitative reverse transcriptase-polymerase chain reaction, in situ hybridization, flow cytometry, and immunohistochemistry, respectively.

MEASUREMENTS AND MAIN RESULTS

Spontaneous CCL18 production by BAL-derived 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 AMs after Th2 cytokine stimulation and/or coculture with human lung fibroblasts. Native collagen significantly up-regulated CCL18 expression in normal AMs activated with Th2 cytokines via a mechanism mediated by beta2-integrin/ scavenger receptor(s). Culture supernatants of AMs from patients with idiopathic pulmonary fibrosis increased collagen production by normal lung fibroblasts partly mediated via CCL18.

CONCLUSIONS

Our findings suggest that AMs 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.

Authors+Show Affiliations

Department of Pneumology, University Hospital, Killianstr. 5, 79106 Freiburg, Germany. prasse@medizin.ukl.uni-freiburg.deNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16415274

Citation

Prasse, Antje, et al. "A Vicious Circle of Alveolar Macrophages and Fibroblasts Perpetuates Pulmonary Fibrosis Via CCL18." American Journal of Respiratory and Critical Care Medicine, vol. 173, no. 7, 2006, pp. 781-92.
Prasse A, Pechkovsky DV, Toews GB, et al. A vicious circle of alveolar macrophages and fibroblasts perpetuates pulmonary fibrosis via CCL18. Am J Respir Crit Care Med. 2006;173(7):781-92.
Prasse, A., Pechkovsky, D. V., Toews, G. B., Jungraithmayr, W., Kollert, F., Goldmann, T., Vollmer, E., Müller-Quernheim, J., & Zissel, G. (2006). A vicious circle of alveolar macrophages and fibroblasts perpetuates pulmonary fibrosis via CCL18. American Journal of Respiratory and Critical Care Medicine, 173(7), 781-92.
Prasse A, et al. A Vicious Circle of Alveolar Macrophages and Fibroblasts Perpetuates Pulmonary Fibrosis Via CCL18. Am J Respir Crit Care Med. 2006 Apr 1;173(7):781-92. PubMed PMID: 16415274.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - A vicious circle of alveolar macrophages and fibroblasts perpetuates pulmonary fibrosis via CCL18. AU - Prasse,Antje, AU - Pechkovsky,Dmitri V, AU - Toews,Galen B, AU - Jungraithmayr,Wolfgang, AU - Kollert,Florian, AU - Goldmann,Torsten, AU - Vollmer,Ekkehard, AU - Müller-Quernheim,Joachim, AU - Zissel,Gernot, Y1 - 2006/01/13/ PY - 2006/1/18/pubmed PY - 2006/10/4/medline PY - 2006/1/18/entrez SP - 781 EP - 92 JF - American journal of respiratory and critical care medicine JO - Am. J. Respir. Crit. Care Med. VL - 173 IS - 7 N2 - RATIONALE: Recently, models of macrophage activation have been revised. Macrophages stimulated with Th2 cytokines have been classified as alternatively activated. OBJECTIVES: This article examines the expression and regulation of CC chemokine ligand 18 (CCL18), a marker of alternative activation, by human alveolar macrophages (AMs). METHODS: AM were obtained from bronchoalveolar lavage (BAL) fluid of patients with idiopathic pulmonary fibrosis, sarcoidosis, or hypersensitivity pneumonitis (n = 69) and healthy volunteers (n = 22). Expression of CCL18 was determined by quantitative reverse transcriptase-polymerase chain reaction, in situ hybridization, flow cytometry, and immunohistochemistry, respectively. MEASUREMENTS AND MAIN RESULTS: Spontaneous CCL18 production by BAL-derived 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 AMs after Th2 cytokine stimulation and/or coculture with human lung fibroblasts. Native collagen significantly up-regulated CCL18 expression in normal AMs activated with Th2 cytokines via a mechanism mediated by beta2-integrin/ scavenger receptor(s). Culture supernatants of AMs from patients with idiopathic pulmonary fibrosis increased collagen production by normal lung fibroblasts partly mediated via CCL18. CONCLUSIONS: Our findings suggest that AMs 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. SN - 1073-449X UR - https://www.unboundmedicine.com/medline/citation/16415274/A_vicious_circle_of_alveolar_macrophages_and_fibroblasts_perpetuates_pulmonary_fibrosis_via_CCL18_ L2 - http://www.atsjournals.org/doi/full/10.1164/rccm.200509-1518OC?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -