Pro-Inflammatory and Anti-Inflammatory Cytokine Expression in Tnf-/- and WT Mice with Chronic Colitis
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Inflammatory Bowel Diseases (IBD) affect approximately 3.6 million people all over the world, mainly in industrialized countries in North America and Europe. The pathogenesis of IBD is incompletely understood, but it is thought to be caused by an exaggerated immune response to the intestinal microbiome in genetically susceptible people. Crohn's Disease (CD), a subtype of IBD, is characterized by recurring bouts of inflammation within the gastrointestinal tract and production of excessive amounts of many proinflammatory cytokines, including tumor necrosis factor (TNF). AntiTNF therapy is a common immunotherapy for patients with CD, however, some patients are either nonresponsive to antiTNF treatment or become nonresponsive over time. The cause of the nonresponsiveness is not known, but may be related to variations in cytokine production or the microbiome. In this study, we use the 2,4,6trinitrobenzenesulfonic acid (TNBS) colitis model to induce chronic, Crohn'slike colitis in WT mice and mice with deletion of the Tnf gene (Tnf/) over a period of five weeks. Spleen and colon samples were collected five weeks post induction of colitis to analyze systemic and local expression levels, respectively, of several proinflammatory and antiinflammatory cytokines. We found that the WT mice had significantly more colitis than the Tnf/ mice, therefore, we hypothesize that WT mice will have higher local and systemic proinflammatory cytokine expression levels and lower antiinflammatory cytokines levels when compared to the Tnf/ mice and that the cytokine levels will correlate with inflammation and alterations in the microbiome.
