A Vicious Circle of Alveolar Macrophages and Fibroblasts Perpetuates Pulmonary Fibrosis via CCL18
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 β2-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.
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Macrophages play a crucial role in the pathogenesis of lung fibrosis.
“Although it has long been recognized that macrophages play a crucial role in the pathogenesis of lung fibrosis”
From TREM2 promotes lung fibrosis via controlling alveolar macrophage survival and pro-fibrotic activity (2025) · cites this paper as [25]
It remains largely unclear what regulates the pro-fibrotic potency of lung macrophages.
“it remains largely unclear what regulates their pro-fibrotic potency in the lung2,3,19–27”
From TREM2 promotes lung fibrosis via controlling alveolar macrophage survival and pro-fibrotic activity (2025) · cites this paper as [25]
CCL18 is involved in recruitment and activation of CD4+ and CD8+ T cells and plays a central role in perpetuating fibrotic processes through a positive feedback loop linking activated macrophages to fibroblasts.
“CCL18 is also known to be involved in the recruitment and activation of CD4+ and CD8+ T cells and, more remarkably, is credited with playing a central role in perpetuating fibrotic processes through its involvement in a positive feedback loop that links activated macrophages to fibroblasts [26].”
From Adipose tissue transcriptomic signature highlights the pathological relevance of extracellular matrix in human obesity (2008) · cites this paper as [26]
CCL18 synthesis by alternatively activated macrophages is induced by Th2 cytokines, ITGB2 and CD163.
“Available data demonstrate that the synthesis of CCL18 by alternatively activated macrophages is induced by Th2 cytokines, integrin beta 2 (ITGB2) and the scavenger receptor (CD163) [26].”
From Adipose tissue transcriptomic signature highlights the pathological relevance of extracellular matrix in human obesity (2008) · cites this paper as [26]
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- Authors
- Prasse, A., Pechkovsky, D. V., Toews, G. B., Jungraithmayr, W., Kollert, F., Goldmann, T., Vollmer, E., Müller-Quernheim, J., & Zissel, G.
- Affiliations
- University of Michigan (US)
- Departments of Pneumology and Thoracic Surgery, University Hospital, Freiburg; Division of Clinical and Experimental Pathology, Research Center, Borstel, Germany; and Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, Michigan
- ORCID
- Venue
- American Journal of Respiratory and Critical Care Medicine
- Publisher
- Oxford University Press (OUP)
- Published
- 2006-04-01
- Volume
- 173
- Issue
- 7
- Pages
- 781-792
- ISSN
- 1073-449X (ISSN-L)
- 1535-4970
- OpenAlex
- W2171849700
- Cited by
- 497
- References
- 57
- Citations by year
- 2026: 20 · 2025: 25 · 2024: 37 · 2023: 38 · 2022: 33 · 2021: 28 · 2020: 27 · 2019: 21 · 2018: 22 · 2017: 26 · 2016: 32 · 2015: 18 · 2014: 20 · 2013: 33 · 2012: 27
- FWCI
- 13.56
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- American Journal of Respiratory and Critical Care Medicine (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Health Sciences › Medicine › Surgery › Transplantation: Methods and Outcomes
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Pulmonary Hypertension Research and Treatments
- Keywords
- CCL18, alveolar macrophages, lung fibroblasts, pulmonary fibrosis, alternative macrophage activation, Th2 cytokines, idiopathic pulmonary fibrosis, sarcoidosis, hypersensitivity pneumonitis, collagen synthesis, beta2 integrins, scavenger receptors, macrophage-fibroblast interaction, positive feedback loop
- MeSH terms
- Biopsy, Bronchoalveolar Lavage Fluid, Cell Line, Fibroblasts, Humans, Immunohistochemistry, Macrophage Activation, Pulmonary Fibrosis, RNA, Messenger, Gene Expression, Cytokines, Macrophages, Alveolar, In Situ Hybridization, Chemokines, CC, Reverse Transcriptase Polymerase Chain Reaction, Collagen Type I, In Vitro Techniques
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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