Abstract
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.
Highlights
Inflammatory bowel disease (IBD) is a complex multifactorial disease [1,2,3]
Dozens of different animal models of IBD have been developed. These models can be broadly divided into spontaneous colitis models, inducible colitis models, genetically modified models, and adoptive transfer models [6,7,8]. These models do not represent the complexity of human disease, they are valuable and indispensable tools that provide a wide range of options for investigating involvement of various factors into the pathogenesis of IBD and evaluate different therapeutic options
The dextran sulphate sodium (DSS-)induced colitis model has some advantages when compared to other animal models of colitis
Summary
Inflammatory bowel disease (IBD) is a complex multifactorial disease [1,2,3]. It commonly refers to ulcerative colitis (UC) and Crohn’s disease (CD), the two chronic conditions that involve inflammation of the intestine. Dozens of different animal models of IBD have been developed These models can be broadly divided into spontaneous colitis models, inducible colitis models, genetically modified models, and adoptive transfer models [6,7,8]. These models do not represent the complexity of human disease, they are valuable and indispensable tools that provide a wide range of options for investigating involvement of various factors into the pathogenesis of IBD and evaluate different therapeutic options. At the same time few aspects of applicability and further investigation of this model are mentioned
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