Figure 1.

IEC function and intestinal homeostasis can be influenced by mitochondrial dysfunction. (A) During intestinal homeostasis, goblet cells produce a healthy mucus layer that protects the IECs from the contents of the lumen, and Paneth cells produce and release antimicrobial peptides to protect IECs. Mitochondria are dense and contain well-formed cristae. The tight junctions inhibit translocation of luminal antigens across the epithelial barrier. Any basal ROS produced is negated by cellular antioxidants. Leukocytes survey the laminia propria for threats. (B) Studies have shown that during the inflammatory conditions of IBD, the mucus layer is reduced and production of antimicrobial peptides is decreased, exposing the intestinal epithelium to the intestinal microbiota and luminal antigens. Mitochondria are swollen and abnormal, and cristae are irregular, resulting in a reduction in ATP production and an increase in ROS. Cellular antioxidants are also decreased, causing a buildup of cellular ROS. There is an increase in epithelial permeability (both transcellular and paracellular) and translocation of bacteria and luminal antigens. This results in an infiltration of immune cells, which also causes an increase of ROS. Both IL-8 and IL-1B are released by immune cells, and immune cell-bacterial interactions further instigates the release of pro-inflammatory mediators, which can feedback onto the IECs and influence other cellular components of the intestinal epithelium.