Necrotizing enterocolitis leads to disruption of tight junctions and increase in gut permeability in a mouse model

Abstract

Abstract Background Necrotizing enterocolitis (NEC) is a leading cause of death in preterm infants. Neonates weighing 50% of experimental pups, pups lost nearly 40% of weight and their intestines showed gross changes and microscopic changes associated with NEC. There were inflammatory changes with loss of tight junction barrier function and disruption of tight junction claudin proteins in the intestines of NEC mouse model. We have demonstrated for the first time that NEC intestines develop increased leakiness as visualized by biotin tracer leakage. Conclusions NEC leads to breakdown of epithelial barrier due to changes in tight junction proteins with increased leakiness which may explain the transmigration of microbes and microbial products from the gut lumen into the blood stream leading to sepsis like signs clinically witnessed.

Keywords

• Necrotizing enterocolitis
• Tight junctions
• Claudin proteins
• Biotin tracer molecules
• Epithelial barrier function