ArticleJOR spine2025
Macrophage Subtypes Distinctly Impact Intervertebral Disc Inflammation and Extracellular Matrix Composition.
Article in JOR spine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Global trends and hotspots of macrophage-related research in intervertebral disc degeneration from 2005 to 2025: a bibliometric and visualized analysis.Frontiers in immunology · 2026Pooled it
- Surviving the Nucleus Pulposus Desert: Next-Generation Strategies for Intervertebral Disc Cell Therapy.JOR spine · 2026Article
- Advancing Basic and Preclinical Spine Research: Highlights From the ORS PSRS 7th International Spine Research Symposium.JOR spine · 2026Article
- Macrophage Subtypes Distinctly Impact Intervertebral Disc Inflammation and Extracellular Matrix Composition.JOR spine · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Background: Intervertebral disc (IVD) degeneration is characterized by changes in extracellular matrix (ECM) composition and an inflammatory microenvironment, including macrophage recruitment. While inflammation is known to amplify ECM degradation, the individual roles of IVD cells and macrophages, and contributions of crosstalk are unknown. Additionally, the impacts of polarized pro-inflammatory M1 or anti-inflammatory M2 macrophages on the IVD are unknown, highlighting a need for an in vitro macrophage-IVD explant co-culture system. Methods: IVDs were dissected from the lumbar spine of rats and cultured encapsulated in agarose. Primary bone marrow-derived macrophages were isolated and polarized to M1 or M2. IVD explants were cultured for 14 days with or without TNFα. M1 or M2 macrophages were co-cultured with unstimulated or TNFα-stimulated IVDs. Changes in ECM were evaluated using glycosaminoglycan (GAG) loss into media, IVD GAG and collagen content, and histology. Inflammatory responses were assessed by measuring nitric oxide (NO) and cytokines (TNFα, IL-6, IL-13, CCL2) in media supernatants. Results: TNFα stimulation of IVDs increased NO, TNFα, and CCL2, indicating an impact on inflammation. TNFα stimulation of IVDs also affected IVD ECM, with changes observed in both GAG and collagen. M1 and M2 co-culture counteracted TNFα-induced changes in collagen content, while macrophage subtypes distinctly modulated inflammation. Specifically, M1 macrophages increased inflammatory cytokines (NO, IL-6), while M2 macrophages decreased pro-inflammatory (NO, TNFα) and increased anti-inflammatory (IL-13) cytokines. Macrophage-IVD crosstalk had unique effects on IL-6 and IL-13 levels compared to IVDs or macrophages cultured alone. Conclusions: Inflammatory stimulation of IVDs and co-culture with macrophages in vitro impacted both inflammation and ECM composition. Both macrophage subtypes reversed TNFα-induced changes in collagen content, while M1 and M2 macrophages had detrimental and protective effects on inflammation, respectively. The macrophage-IVD explant co-culture model in this study provides a novel system for evaluating crosstalk exclusively through paracrine signaling.
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