ArticlePloS one2026
Pulmonary fibroblasts activated by the addition of TNF-α and IL-4 enhance lymphangiogenic capacity and ameliorate lung fibrosis in an allogeneic rat model.
Article in PloS one, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundPulmonary fibrosis remains a major clinical challenge with limited treatment options. Recent studies have suggested that fibroblasts, when stimulated by specific cytokines, may acquire lymphangiogenic and antifibrotic properties contributing to tissue repair.
methodsHuman and rat pulmonary fibroblasts (PFs) were stimulated with TNF-α and IL-4 to induce lymphangiogenic and antifibrotic characteristics. In vitro analyses assessed gene expression, cytokine secretion, tube formation capacity, and immunogenicity. Therapeutic efficacy was evaluated in a rat model of bleomycin-induced pulmonary fibrosis following allogeneic PF transplantation.
resultsCytokine-stimulated PFs exhibited upregulation of ADM and VEGFC, enhanced tube formation capacity, and minimal expression of immunogenic markers. In vivo, allogeneic PF transplantation significantly reduced fibrotic lesion and plasma SP-D levels compared to controls. Gene expression analyses demonstrated downregulation of fibrosis-associated markers after treatment.
conclusionCytokine-stimulated pulmonary fibroblasts may serve as a novel cell source for antifibrotic therapy by modulating lymphangiogenesis and tissue remodeling, providing a potential alternative to conventional stem cell-based approaches for fibrotic lung diseases.
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