ArticleRespiratory research2025
Variable steady inflammation and inflammatory responses in precision-cut lung slices from various IPF lung Regions.
Article in Respiratory research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Review
- MAGL-18c attenuates LPS-induced sepsis-associated liver injury by inhibiting TGF-β/Smad signaling and remodeling medium- and long-chain fatty acid metabolism.Frontiers in immunology · 2026Article
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Authors and funding
7 authors.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundThe role of inflammation in the pathogenesis of idiopathic pulmonary fibrosis (IPF) remains controversial. While immune activation is evident in IPF lungs, immunosuppressive therapies have historically been associated with adverse outcomes. Investigating the transcriptional response of IPF lung tissue to inflammatory stimuli may help elucidate the contribution of dysregulated inflammatory pathways to the underlying disease mechanism.
methodsTo test the inflammatory response of IPF lung tissue, human precision-cut lung slices (PCLS) were generated from 3 different regions of IPF lungs: non-fibrotic (NF), transition (T), and dense fibrotic area (F). For control, we obtained PCLS from normal lung tissue (N). PCLS were incubated with or without 100 ng/ml of lipopolysaccharide (LPS) for 48 h. Bulk RNA sequencing was performed and evaluated by differential gene expression (DGE), gene ontology (GO), gene set enrichment analysis (GSEA) and network analysis. Cytokines levels in supernatants, such as tumour necrosis factor (TNF), interleukin (IL)-6 and IL-8, were quantified by ELISA.
resultsOur findings confirm metabolic reprograming, including suppression of fatty acid/cholesterol metabolism and ribosomal genes, as characteristic hallmark of all IPF regions compared to N tissues, with a fibrosis severity-dependent gradient. Interestingly, untreated NF- and T-IPF PCLS showed upregulated inflammatory genes associated with toll-like receptors (TLR), TNF and IL-6 signature when compared to N and F-IPF. However, when challenged with LPS, most of the inflammatory genes displayed attenuated activation in IPF tissues, such as markers for T cells activation (INF-γ and α, TNF via NF-κB, TLR). TNF release was greater in N tissue compared to NF- and T-IPF but less for IL-6 and IL-8 if compared to IPF tissue.
conclusionOur findings show steady inflammation in normal appearing and transitional areas of IPF lung tissue. These inflammatory markers equally participate in the pro-fibrotic signalling through signal transducers and transcription factors, which might result in dual pro-fibrotic and inflammatory effects during disease progression.
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