Cited by 232Interstitial Lung Diseases and Idiopathic Pulmonary FibrosisTransplantation: Methods and OutcomesLiver physiology and pathology

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Modulation of alveolar macrophage-driven fibroblast proliferation by alternative macrophage mediators

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Bitterman, P B, Wewers, M D, Rennard, S I, Adelberg, S, Crystal, R G·1986·Journal of Clinical Investigation

DOI 10.1172/jci112364PMC PMC423453

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Abstract

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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Authors: Bitterman, P. B., Wewers, M. D., Rennard, S. I., Adelberg, S., & Crystal, R. G.
Affiliations: National Institutes of Health (US)
ORCID: Bitterman, P B
Wewers, M D
Rennard, S I
Crystal, R G
Venue: Journal of Clinical Investigation
Publisher: American Society for Clinical Investigation
Published: 1986-03-01
Volume: 77
Issue: 3
Pages: 700-708
ISSN: 0021-9738 (ISSN-L)
DOI: 10.1172/jci112364
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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Modulation of alveolar macrophage-driven fibroblast proliferation by alternative macrophage mediators

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