Inflammatory Bowel Disease (IBD)
Inflammatory bowel diseases (IBDs), primarily ulcerative colitis and Crohn's disease, are inflammatory disorders of the gastrointestinal tract caused by multiple factors involving abnormal gut microbiota, immune response dysregulation and environmental factors. The pathogenesis of IBD is not fully elucidated, but is proposed to implicate immunological factors such as cytokines (e.g. IL-1β, IL-6, IL-18, TNFα and IL-17), TH17 cells, innate lymphoid cells and monocytes/macrophages. As such, therapies targeting cytokines and immune cells can potentially be used for IBD treatment. To induce acute IBD, mice were given libitum access to Dextran Sodium Sulfate (DSS) dissolved in drinking water for 8-10 days or intra-rectal administration of 2,4,6-trinitrobenzene sulphonic acid (TNBS). Body weight, stool quality, and a disease activity index (DAI) score were used to evaluate the clinical progression of colitis. The DAI is the combined score of weight loss compared to initial weight, stool consistency, and fecal blood occurrence.
How it is constructed:
Readouts:
Body weight, stool quality, colon length, histopathological assessment and a Disease Activity Index (DAI) score will be used to evaluate the clinical progression of colitis.
Data - IBD Induction with DSS
Treatment of 2% DSS showed drastic weight reduction and increased the DAI score which is highly associated to the severity of IBD disease symptoms such as body weight loss, diarrhea and fecal blood in stool.
A
The colon length of DSS treated mice is significantly shorter than untreated group.
B
DSS-treatment resulted in immune cell infiltration in colon, degradation of mucus layer and damages the colon integrity. There is greater CD4+ T cells than CD8+ T cells infiltration to colon in area of “ulceration” (arrow).
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