Dextran sulfate sodium induced colitis model

Cooper, H.S. et al.. The role of mutant Ape in the development of dysplasia and cancer in the mouse model of dextran sulfate sodium-induced colitis, Gastroenterology, 121 (6), 1407, 2001. 

CB2-receptors also exist, in low levels, in cells of the gastrointestinal and cardiovascular system, bone and neuronal cells, liver tissue, and other ceU types [26]. CB2 is up-regulated in inflamed colonic tissue of colitis patients. It is believed that the CB2-receptors are in close interaction with the PPARy-receptor, and both are considered targets for treatment of inflammatory bowel diseases. That was the motivation for Bento et al. [27] to investigate the effect of oral BCP in DSS (dextran sulfate sodium)-induced colitis experimental models. The results showed that BCP inhibited the influx of inflammatory cells. 

Helminths may not inhibit or modulate all types of inflanunation. Mice with oxazalone colitis, another model of intestinal inflammation, develop worse disease if colonized with the tape worm Hymenolepis diminuta. Yet, exposure to this helminth protects fi om TNBS-like colitis and improves some aspects of dextran sulfate sodium (DSS) colitis. Similarly, mice with mixed-sex S. mansoni infections are more susceptible to DSS-induced colitis relative to uninfected mice, while schistosome male worm-only infections are refraaory to DSS colitis. ... 

OA were aborted in 2003 due to the development of mild to moderate liver fibrosis in dogs treated for 9 months with high doses of pralnacasan. This was in spite of recent evidence demonstrating the effectiveness of pralnacasan treatment in the acute dextran sulfate sodium (DSS)-induced colitis model, which resembles Crohn s disease (CD) characteristics, and in transient ischemia induced brain damage. 

The second example of what might be considered to be an unexpected D6 null phenotype came from our studies using the dextran sodium sulfate (DSS)-induced model of colitis [29]. D6 is abundantly expressed in the colon and upregulated during colitis in wildtype mice. However, we found that D6 null mice had a reduced tendency to develop the clinical symptoms of colitis compared to their wildtype counterparts, and had neither altered levels of bioavailable inflammatory CC chemokines nor... 

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