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Modulation of alveolar macrophage-driven fibroblast proliferation by alternative macrophage mediators
Open accessAbstract
Tissue fibrosis results, in part, from an interaction between growth regulatory molecules released by mononuclear phagocytes and fibroblasts. In the chronic interstitial lung disorders, alveolar macrophages, the mononuclear phagocytes of the lung, are known to spontaneously release two growth factors for fibroblasts, fibronectin and alveolar macrophage-derived growth factor (AMDGF) that together stimulate nonreplicating lung fibroblasts to divide. In addition to these two primary growth promoting signals, alveolar macrophages are able to release other mediators that may have a potential role in modulating lung fibroblast replication in response to these primary signals, including interferon gamma (IFN gamma), prostaglandin E2 (PGE2), and interleukin 1 (IL-1). To evaluate this possibility, we examined the effect of each of these other mediators on lung fibroblast replication in response to fibronectin and AMDGF in serum-free, defined medium. IFN gamma had no effect on fibroblast replication. In contrast, PGE2 resulted in a dose-dependent inhibition of fibroblast replication in response to fibronectin and AMDGF with 50% of the maximum inhibition observed at a PGE2 concentration of less than 10 ng/ml. IL-1, while not active as a primary growth promoting signal, at concentrations of 4-10 U/ml, augmented fibroblast replication in response to fibronectin and AMDGF by 10 to 15%. Temporally, the growth augmenting effect of IL-1 occurred early in the G1 phase of the cell cycle. These data indicate that lung fibroblast replication in response to two of the primary growth promoting signals spontaneously released by alveolar macrophages in the interstitial lung disorders, while uninfluenced by IFN gamma, can be inhibited by PGE2 and modestly augmented by IL-1. Understanding the relevant fibroblast growth modulatory signals within the alveolar microenvironment in the chronic interstitial disorders may lead to rational therapeutic strategies designed to interrupt the fibrotic process.
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“alveolar macrophages obtained from patients with IPF were shown to stimulate fibroblast accumulation via a paracrine mechanism involving the production of soluble mediators typically associated with alternative activation (18)”
From The Role of Immune and Inflammatory Cells in Idiopathic Pulmonary Fibrosis (2018) · cites this paper as [18]
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Metadata
- Authors
- Bitterman, P. B., Wewers, M. D., Rennard, S. I., Adelberg, S., & Crystal, R. G.
- Affiliations
- National Institutes of Health (US)
- Venue
- Journal of Clinical Investigation
- Published
- 1986-03-01
- Volume
- 77
- Issue
- 3
- Pages
- 700-708
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC423453
- OpenAlex
- W1971418747
- Cited by
- 232
- References
- 50
- Citations by year
- 2025: 1 · 2024: 2 · 2023: 1 · 2021: 4 · 2020: 2 · 2019: 5 · 2018: 2 · 2017: 3 · 2016: 2 · 2015: 2 · 2014: 2 · 2013: 3 · 2012: 6
- FWCI
- 19.57
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (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 › Hepatology › Liver physiology and pathology
- Keywords
- alveolar macrophages, lung fibroblast proliferation, fibrosis, fibronectin, prostaglandin E2, interleukin-1, interferon-gamma, G1 phase
- MeSH terms
- Cell Cycle, Culture Media, Fibroblasts, Fibronectins, Growth Substances, Humans, Interferon-gamma, Interleukin-1, Lung, Macrophages, Peptides, Prostaglandins E, Pulmonary Fibrosis, Time Factors, Dinoprostone, Intercellular Signaling Peptides and Proteins
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