ArticleInflammatory bowel diseases2011
Role of tumor necrosis factor-α in the extraintestinal thrombosis associated with colonic inflammation.
Article in Inflammatory bowel diseases, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 49 citations in OpenAlex.
- Decreases in colonic and systemic inflammation in chronic HIV infection after IL-7 administration.PLoS pathogens · 2014Trial
- Extraintestinal Manifestations of Inflammatory Bowel Disease: A Focus on Kidney Complications.International journal of molecular sciences · 2026Review
- Neutrophils and NETs in Pathophysiology and Treatment of Inflammatory Bowel Disease.International journal of molecular sciences · 2025Review
- Relationship between venous thromboembolism and inflammatory bowel disease in Taiwan: a nationwide retrospective cohort study.BMC cardiovascular disorders · 2025Article
- Exosomes-transferred LINC00668 Contributes to Thrombosis by Promoting NETs Formation in Inflammatory Bowel Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Platelet factor 4 is a biomarker for lymphatic-promoted disorders.JCI insight · 2020Article
- Venous thromboembolism in inflammatory bowel disease.World journal of gastroenterology · 2020Review
- TNF-α-driven inflammation and mitochondrial dysfunction define the platelet hyperreactivity of aging.Blood · 2019Article
- Article
- Administration ofFrontiers in microbiology · 2019Article
- Fibrinogen-like protein 2 prothrombinase may contribute to the progression of inflammatory bowel disease by mediating immune coagulation.International journal of clinical and experimental pathology · 2018Article
- Levels and activities of von Willebrand factor and metalloproteinase with thrombospondin type-1 motif, number 13 in inflammatory bowel diseases.World journal of gastroenterology · 2017Article
- Targeting factor VIII expression to platelets for hemophilia A gene therapy does not induce an apparent thrombotic risk in mice.Journal of thrombosis and haemostasis : JTH · 2017Article
- Thromboembolic complications in inflammatory bowel disease.Journal of thrombosis and thrombolysis · 2015Review
- MyD88 mediates the protective effects of probiotics against the arteriolar thrombosis and leukocyte recruitment associated with experimental colitis.Inflammatory bowel diseases · 2015Article
- Systemic and flap inflammatory response associates with thrombosis in flap venous crisis.Inflammation · 2015Article
- Venous thrombosis and prothrombotic factors in inflammatory bowel disease.World journal of gastroenterology · 2014Review
- Platelet activation and platelet-leukocyte aggregation elicited in experimental colitis are mediated by interleukin-6.Inflammatory bowel diseases · 2014Article
- Possible association of etanercept, venous thrombosis, and induction of antiphospholipid syndrome.Case reports in rheumatology · 2014Article
- Interleukin-6 mediates the platelet abnormalities and thrombogenesis associated with experimental colitis.The American journal of pathology · 2013Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundInflammatory bowel diseases (IBDs) are associated with a hypercoagulable state and an increased risk of thromboembolism, with accelerated thrombus formation occurring both within the inflamed bowel and in distant tissues. While the IBD-associated prothrombogenic state has been linked to the inflammatory response, the mediators that link inflammation and thrombosis remain poorly defined. The objective of this study was to assess the role of tumor necrosis factor alpha (TNF-α) in the enhanced extraintestinal microvascular thrombosis that accompanies colonic inflammation.
methodsTNF-α concentration was measured in plasma, colon, and skeletal muscle of control mice and in mice with dextran sodium sulfate (DSS)-induced colitis. A light/dye injury method was used to induce microvascular thrombosis in cremaster microvessels. The effects of exogenous TNF-α on thrombus formation were determined in control mice. DSS-enhanced thrombus formation was evaluated in wildtype (WT) mice treated with an anti-TNF-α antibody (±an anti-IL-1β antibody) and in TNF-α receptor-deficient (TNFr(-/-) ) mice.
resultsDSS colitis enhanced thrombus formation in cremaster arterioles. A similar response was produced by TNF-α administration in control mice. TNF-α concentration was elevated in plasma, colon, and skeletal muscle. Immunoblockade of TNF-α or genetic deficiency of the TNF-α receptor blunted the thrombotic response of arterioles to DSS colitis. Additional protection was noted in mice receiving antibodies to both TNF-α and IL-1β.
conclusionsOur findings implicate TNF-α in the enhanced microvascular thrombosis that occurs in extraintestinal tissue during colonic inflammation, and suggests that the combined actions of TNF-α and IL-1β accounts for most of the colitis-enhanced thrombotic response.
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