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Previous studies of intestinal inflammation have identified aberrant pathways that disrupt the homeostasis of the intestinal microenvironment. Loss of intestinal epithelial cell (IEC) barrier function, microbiota infiltration, and epithelial regeneration have been well characterized and correlated with dysregulated inflammatory responses in both patients and murine models (1). The role metabolic pathways play during the pathogenesis of inflammatory bowel disease (IBD), however, is not well-defined due to the multifaceted interaction during the disease progression between the host’s IECs, microbiota, immune cells, location, and environment (2). Treatment of IBD includes targeting multiple proinflammatory cytokines, including TNFa and IL-17A (3). While anti-IL-17A antibody therapy failed in clinical trials, anti-TNFa antibodies, such as infliximab and adalimumab, are now established treatments of IBD (4).

digestive medicine research

Aberrant differentiation of intestinal stem cells due to inflammation-induced mitochondrial dysfunction predicts postoperative recurrence of Crohn’s disease