ArticleImmunology2017
Ficolin-A/2, acting as a new regulator of macrophage polarization, mediates the inflammatory response in experimental mouse colitis.
Article in Immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 45 citations in OpenAlex.
- NMI Promotes Pro-Inflammatory Macrophage Polarization and Exacerbates.Inflammation · 2026Article
- Panoramic description of ROS-based nanotechnology for osteomyelitis therapy: Challenges, opportunities, and prospects.Theranostics · 2026Review
- Species differences in opsonization and phagocyte recognition of preclinical poly-2-alkyl-2-oxazoline-coated nanoparticles.Nature communications · 2025Article
- Ficolin-A induces macrophage polarization to a novel pro-inflammatory phenotype distinct from classical M1.Cell communication and signaling : CCS · 2024Article
- Chensinin-1b Alleviates DSS-Induced Inflammatory Bowel Disease by Inducing Macrophage Switching from the M1 to the M2 Phenotype.Biomedicines · 2024Article
- The Lectin Pathway of the Complement System-Activation, Regulation, Disease Connections and Interplay with Other (Proteolytic) Systems.International journal of molecular sciences · 2024Review
- Macrophage polarization in inflammatory bowel disease.Cell communication and signaling : CCS · 2023Review
- Ficolin-2 amplifies inflammation in macrophage-smooth muscle cell cross-talk and increases monocyte transmigration by mechanisms involving IL-1β and IL-6.Scientific reports · 2023Article
- Ficolin-2: A potential immune-related therapeutic target with low expression in liver cancer.Frontiers in oncology · 2022Article
- The ATP-hydrolyzing ectoenzyme E-NTPD8 attenuates colitis through modulation of P2X4 receptor-dependent metabolism in myeloid cells.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Autotaxin stimulates LPA2 receptor in macrophages and exacerbates dextran sulfate sodium-induced acute colitis.Journal of molecular medicine (Berlin, Germany) · 2020Article
- Gut microbial bile acid metabolite skews macrophage polarization and contributes to high-fat diet-induced colonic inflammation.Gut microbes · 2020Article
- Mannose-capped lipoarabinomannan-induced B10 cells decrease severity of dextran sodium sulphate-induced inflammatory bowel disease in mice.Scandinavian journal of immunology · 2020Article
- Myricetin Modulates Macrophage Polarization and Mitigates Liver Inflammation and Fibrosis in a Murine Model of Nonalcoholic Steatohepatitis.Frontiers in medicine · 2020Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human ficolin-2 (FCN-2) and mouse ficolin-A (FCN-A, a ficolin-2-like molecule in mouse) are activators of the lectin complement pathway, present in normal plasma and usually associated with infectious diseases, but little is known about the role of FCN-A/2 in inflammatory bowel disease (IBD). In our present study, we found that patients with IBD exhibited much higher serum FCN-2 levels than healthy controls. In the dextran sulphate sodium-induced acute colitis mouse model, FCN-A knockout mice showed much milder disease symptoms with less histological damage, lower expression levels of pro-inflammatory cytokines [interleukin-6 (IL-6), IL-1β and tumour necrosis factor-α (TNF-α)], chemokines (CXCL1/2/10 and CCL4) and higher levels of the anti-inflammatory cytokine IL-10 compared with wild-type mice. We demonstrated that FCN-A/2 exacerbated the inflammatory pathogenesis of IBD by stimulating M1 polarization through the TLR4/MyD88/MAPK/NF-κB signalling pathway in macrophages. Hence, our data suggest that FCN-A/2 may be used as a novel therapeutic target for IBD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.