ArticleCell communication and signaling : CCS2024
Ficolin-A induces macrophage polarization to a novel pro-inflammatory phenotype distinct from classical M1.
Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Melanoma stem cells drive macrophage reprogramming to a hybrid phenotype, modulating melanoma stemness and compromising NK cell-mediated immunity.Frontiers in immunology · 2026Article
- The Role of IFN-γ-Mediated Immune Cell Crosstalk in the Pathogenesis of Aplastic Anemia.Journal of immunology research · 2026Review
- Wenshen Zhuanggu Fang reduces breast cancer bone metastasis by regulating macrophage polarization: a bioinformatics analysis combined with experimental validation.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2025Article
- Platelet-derived exosomes in situ reprogramming macrophages for rheumatoid arthritis treatment.Cell communication and signaling : CCS · 2025Article
- The ADAMTS2 metalloproteinase inhibits tumor growth by regulating the innate immune system.Cancer cell international · 2025Article
- Autophagy-related biomarkers identified in sepsis-induced ARDS through bioinformatics analysis.Scientific reports · 2025Article
- Differential Expression of ARG1 and MRC2 in Retinal Müller Glial Cells During Autoimmune Uveitis.Biomolecules · 2025Article
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Abstract
backgroundMacrophages are key inflammatory immune cells that orchestrate the initiation and progression of autoimmune diseases. The characters of macrophage in diseases are determined by its phenotype in response to the local microenvironment. Ficolins have been confirmed as crucial contributors to autoimmune diseases, with Ficolin-2 being particularly elevated in patients with autoimmune diseases. However, whether Ficolin-A stimulates macrophage polarization is still poorly understood.
methodsWe investigated the transcriptomic expression profile of murine bone marrow-derived macrophages (BMDMs) stimulated with Ficolin-A using RNA-sequencing. To further confirm a distinct phenotype activated by Ficolin-A, quantitative RT-PCR and Luminex assay were performed in this study. Additionally, we assessed the activation of underlying cell signaling pathways triggered by Ficolin-A. Finally, the impact of Ficolin-A on macrophages were investigated in vivo through building Collagen-induced arthritis (CIA) and Dextran Sulfate Sodium Salt (DSS)-induced colitis mouse models with Fcna-/- mice.
resultsFicolin-A activated macrophages into a pro-inflammatory phenotype distinct to LPS-, IFN-γ- and IFN-γ + LPS-induced phenotypes. The transcriptomic profile induced by Ficolin-A was primarily characterized by upregulation of interleukins, chemokines, iNOS, and Arginase 1, along with downregulation of CD86 and CD206, setting it apart from the M1 and M2 phenotypes. The activation effect of Ficolin-A on macrophages deteriorated the symptoms of CIA and DSS mouse models, and the deletion of Fcna significantly alleviated the severity of diseases in mice.
conclusionOur work used transcriptomic analysis by RNA-Seq to investigate the impact of Ficolin-A on macrophage polarization. Our findings demonstrate that Ficolin-A induces a novel pro-inflammatory phenotype distinct to the phenotypes activated by LPS, IFN-γ and IFN-γ + LPS on macrophages.
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