ArticleDigestive diseases and sciences2021
Thalidomide Attenuates Colitis and Is Associated with the Suppression of M1 Macrophage Polarization by Targeting the Transcription Factor IRF5.
Article in Digestive diseases and sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 17 citations in OpenAlex.
- Review
- Ulcerative colitis: signaling pathways, therapeutic targets and interventional strategies.Signal transduction and targeted therapy · 2026Review
- Review on advances in small molecule inhibitors on the treatment of inflammatory bowel disease.Molecular biology reports · 2026Review
- Development and functional adaptation of intestinal macrophages across the lifespan.Clinical & translational immunology · 2026Review
- The YAP/TEAD4 transcriptional complex in intestinal macrophages promotes M2 polarization and alleviates DSS-induced colitis via the regulation of C/EBPβ.Scientific reports · 2025Article
- TRIM21 regulation of IRF-mediated type I interferon signaling in systemic autoimmune diseases.Frontiers in immunology · 2025Review
- Ulcerative colitis: the healing power of macrophages.Tissue barriers · 2025Review
- The multiple roles of interferon regulatory factor family in health and disease.Signal transduction and targeted therapy · 2024Review
- Inflammatory bowel disease and rheumatoid arthritis share a common genetic structure.Frontiers in immunology · 2024Article
- Update and latest advances in mechanisms and management of colitis-associated colorectal cancer.World journal of gastrointestinal oncology · 2023Review
- Overcoming cancer risk in inflammatory bowel disease: new insights into preventive strategies and pathogenesis mechanisms including interactions of immune cells, cancer signaling pathways, and gut microbiota.Frontiers in immunology · 2023Review
- Exosome-mediated macrophage regulation for inflammatory bowel disease repair: a potential target of gut inflammation.American journal of translational research · 2023Review
- Oral Administration of Cryptotanshinone-Encapsulated Nanoparticles for the Amelioration of Ulcerative Colitis.Cellular and molecular bioengineering · 2022Article
- YAP Activates STAT3 Signalling to Promote Colonic Epithelial Cell Proliferation in DSS-Induced Colitis and Colitis Associated Cancer.Journal of inflammation research · 2022Article
- The Role of Tissue-Resident Macrophages in the Development and Treatment of Inflammatory Bowel Disease.Frontiers in cell and developmental biology · 2022Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundUlcerative colitis (UC) is a chronic inflammatory bowel disease. The TNF-α inhibitor thalidomide is reported to be effective for inducing remission in pediatric Crohn's disease (CD) and adults with refractory CD. The mechanisms underlying the immunomodulatory and anti-inflammatory properties of thalidomide are unclear.
methodsHistological assessments were firstly performed in thalidomide treated UC patients. Then the effect of thalidomide in vivo was detected in DSS-induced murine colitis. The mechanism involving IRF5, and M1 macrophage polarization was investigated by using plasmid transfection, western blotting, and real-time PCR. Finally, AOM/DSS model was used to detect the role of thalidomide in colitis associated cancer.
resultsWe first found that treatment with thalidomide could ameliorate colon inflammation for 8 weeks and promote mucosal healing in human UC. Moreover, treatment with thalidomide protected mice from dextran sodium sulfate (DSS)-induced acute colitis, with treated mice presenting with a higher body weight, lower histological score, and lower DAI. Concomitantly, in comparison with control mice, mice treated with thalidomide showed accelerated recovery following colitis after 10 days of thalidomide treatment. Mechanistically, we observed that thalidomide could increase epithelial cell self-renewal capacity and modulate M1/M2 polarization by decreasing M1 markers CD86 and CCR7 and increasing M2 protein signatures CD206 and Arg-1. Thalidomide controls M1 macrophage polarization by targeting the transcription factor IRF5. Finally, by using the classical AOM/DSS model, we found that thalidomide-treated mice presented with a lower incidence and growth of colitis-associated carcinoma (CAC) than negative control mice.
conclusionsIn summary, thalidomide suppresses M1 polarization in the inflammatory microenvironment, which not only attenuates colonic inflammation to facilitate mucosal healing after DSS-induced injury but also represses the progression of CAC.
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