RESEARCH PAPER
Lunasin influences macrophage–pulmonary epithelial crosstalk in cellular model of hypersensitivity pneumonitis
 
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Department of Medical Biology, Institute of Rural Health, Lublin, Poland
 
 
Corresponding author
Michał Chojnacki   

Department of Medical Biology, Institute of Rural Health, Lublin, Jaczewskiego 2, 20-090, Lublin, Poland
 
 
 
KEYWORDS
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ABSTRACT
Introduction and objective:
Hypersensitivity pneumonitis (HP) is a chronic immune-mediated interstitial lung disease driven by persistent antigen exposure, macrophage activation, and progressive lung remodelling. Macrophage-derived transforming growth factor beta (TGF-β) plays a key role in epithelial–mesenchymal transition (EMT), contributing to fibrosis development. Lunasin, a soybean-derived bioactive peptide, exhibits anti-inflammatory and immunomodulatory properties, but its influence on macrophage–epithelial interactions in HP remains unclear. The aim of the study is to evaluate the effects of lunasin on antigen-induced macrophage activation, TGF-β secretion, and macrophage-driven EMT in a long-term in vitro model of HP.

Material and methods:
SC macrophages were chronically stimulated with Pantoea agglomerans antigen in the presence or absence of lunasin (50 µM). Viability (MTT), macrophage polarization (flow cytometry), and TGF-β secretion (CBA assay) were assessed. NL20 bronchial epithelial cells were exposed to macrophage-conditioned media, and morphological changes and EMT marker expression were analyzed.

Results:
Lunasin attenuated antigen-induced M1 polarization at later time points but did not significantly alter TGF-β levels in PA-stimulated macrophages. Conditioned media from antigen-activated macrophages induced EMT-like changes in epithelial cells, including altered morphology and increased mesenchymal marker expression. Media derived from lunasin-treated macrophages partially preserved epithelial morphology and produced limited, marker-specific changes in EMT-associated proteins.

Conclusions:
Lunasin modulates antigen-induced macrophage activation and influences macrophage–epithelial crosstalk in vitro, attenuating selected profibrotic and EMT-associated responses relevant to HP-related lung remodelling.
ACKNOWLEDGEMENTS
The study was supported by the Institute of Rural Health in Lublin, Poland, under Project No. 22020: ‘The role of lunasin in epithelial-mesenchymal transition in pulmonary fibrosis in the course of hypersensitivity pneumonities – studies in an in vitro model”.
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