The role of the complement and contact systems in the dextran sulfate sodium-induced colitis model: the effect of C1 inhibitor in inflammatory bowel disease

Lu, Fengxin; Fernandes, Stacey M.; Davis, Alvin E.

doi:10.1152/ajpgi.00400.2009

Cited by 35 publications

(28 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These include cytokines, eicosanoids, reactive oxygen species, nitric oxide, and complement system activation products [45–48]. Similarly, DSS-induced colitis is associated with the upregulation of different cytokines, chemokines, nitric oxide [49, 50], and inducible nitric oxide synthase (iNOS) [51].…”

Section: Pathogenesis Of Dss-induced Colitismentioning

confidence: 99%

Dextran Sodium Sulphate Colitis Mouse Model: Traps and Tricks

Perše

Cerar

2012

Journal of Biomedicine and Biotechnology

730

674

View full text Add to dashboard Cite

Inflammatory bowel disease (IBD) is a complex multifactorial disease of unknown etiology. Thus, dozens of different animal models of IBD have been developed in past decades. Animal models of IBD are valuable and indispensable tools that provide a wide range of options for investigating involvement of various factors into the pathogenesis of IBD and to evaluate different therapeutic options. However, the dextran sulphate sodium (DSS-) induced colitis model has some advantages when compared to other animal models of colitis. It is well appreciated and widely used model of inflammatory bowel disease because of its simplicity. It has many similarities to human IBD, which are mentioned in the paper. In spite of its simplicity and wide applicability, there are also traps that need to be taken into account when using DSS model. As demonstrated in the present paper, various factors may affect susceptibility to DSS-induced lesions and modify results.

show abstract

Section: Pathogenesis Of Dss-induced Colitismentioning

confidence: 99%

Dextran Sodium Sulphate Colitis Mouse Model: Traps and Tricks

Perše

Cerar

2012

Journal of Biomedicine and Biotechnology

730

674

View full text Add to dashboard Cite

show abstract

Section: Coagulation and Complementmentioning

confidence: 99%

“…For example, rheumatoid arthritis [134], inflammatory bowel disease [135], and the inflammatory skin conditions urticaria and psoriasis [136] can be characterized by a thrombotic phenotype. Some of this work has pointed to a role for complement activation in the pathogenesis of acute dextran sulfate sodium (DSS)-induced colitis [135], supporting the potential involvement of complement and coagulation in inflammatory bowel disease (IBD). In principle, complement activation in these conditions can facilitate the release of proinflammatory modulators such as C5a and TNF-α, which can in turn also induce a TF-dependent initiation of coagulation [77, 78].…”

Section: Coagulation and Complementmentioning

confidence: 99%

“…A negative role for C1INH in inflammation and coagulation has been also demonstrated in baboons experiencing lethal E. coli sepsis, with inhibitor-treated animals exhibiting reduced amounts of several cytokines such as TNF, IL-10, IL-6, and IL-8 [157]. Interestingly, C1INH administration has recently been shown to ameliorate DSS-induced colitis via a mechanism that involves suppression of leukocyte infiltration [135]. However, this study failed to single out the direct inhibition of the complement or coagulation cascade as the major cause of the C1INH-mediated favorable outcome of this disease.…”

Section: Coagulation and Complementmentioning

confidence: 99%

See 1 more Smart Citation

Interactions between coagulation and complement—their role in inflammation

et al. 2011

View full text Add to dashboard Cite

The parallel expression of activation products of the coagulation, fibrinolysis, and complement systems has long been observed in both clinical and experimental settings. Several interconnections between the individual components of these cascades have also been described, and the list of shared regulators is expanding. The coexistence and interplay of hemostatic and inflammatory mediators in the same microenvironment typically ensures a successful host immune defense in compromised barrier settings. However, dysregulation of the cascade activities or functions of inhibitors in one or both systems can result in clinical manifestations of disease, such as sepsis, systemic lupus erythematosus, or ischemia–reperfusion injury, with critical thrombotic and/or inflammatory complications. An appreciation of the precise relationship between complement activation and thrombosis may facilitate the development of novel therapeutics, as well as improve the clinical management of patients with thrombotic conditions that are characterized by complement-associated inflammatory responses.

show abstract

“…These indicated that other factors in the complement system might also be associated with uveitis. C1 inhibitor (C1INH), a member of the serpin family, is the most important inhibitor of the complement classical pathway, which is involved in the mediation of inflammation and has been shown to be beneficial in a variety of animal models of inflammatory disease, including sepsis, inflammatory bowel disease, ischemia-reperfusion injury, endothelial cell injury, hyperacute transplant rejection and burn injury 11 12. Moreover, the gene encoding C1INH, SERPING1 , has been shown to be associated with a range of inflammatory diseases, such as age-related macular degeneration (AMD) and hereditary angioedema 13–16.…”

Section: Introductionmentioning

confidence: 99%