| First Author | Yoshida H | Year | 2010 |
| Journal | Am J Pathol | Volume | 177 |
| Issue | 6 | Pages | 2774-81 |
| PubMed ID | 20971730 | Mgi Jnum | J:170780 |
| Mgi Id | MGI:4947339 | Doi | 10.2353/ajpath.2010.100205 |
| Citation | Yoshida H, et al. (2010) Interleukin-1beta mediates the extra-intestinal thrombosis associated with experimental colitis. Am J Pathol 177(6):2774-81 |
| abstractText | Inflammatory bowel diseases (IBDs) are associated with an increased risk for thromboembolism, which is often manifested as deep vein thrombosis or pulmonary embolism, at extra-intestinal sites. Although some of the cytokines that contribute to IBD pathogenesis are also known to alter the coagulation pathway, it remains unclear whether these mediators also contribute to the extra-intestinal thrombosis often associated with IBD. The objective of this study is to evaluate the role of interleukin (IL)-1beta in enhanced extra-intestinal thrombosis observed in mice with dextran sodium sulfate (DSS)-induced colitis. IL-1beta concentrations were measured in plasma, colon, and skeletal muscle of wild-type (WT) control and colitic mice. Microvascular thrombosis was induced in cremaster muscle microvessels by using a light/dye injury model. The effects of exogenous IL-1beta on thrombus formation were determined in control WT mice. DSS-induced thrombogenesis was evaluated in WT mice treated with an IL-1beta antibody and in IL-1 receptor-deficient (IL-1r(-/-)) mice. DSS-induced colonic inflammation in WT mice was associated with enhanced thrombus formation in arterioles. IL-1beta concentrations were elevated in inflamed colon and skeletal muscle. Exogenous IL-1beta enhanced thrombosis in control mice in a dose-dependent manner. DSS colitic mice treated with the IL-1beta antibody as well as IL-1r(-/-) mice exhibited significantly blunted thrombogenic responses. These findings implicate IL-1beta as a mediator of enhanced microvascular thromboses that occur in extra-intestinal tissues during colonic inflammation. |
