Journal d'immunologie clinique et cellulaire
Libre accès
ISSN: 2155-9899
ISSN: 2155-9899
Tamas Jilling, Jing Lu and Michael S. Caplan
Necrotizing enterocolitis is one of the most severe, life-threatening consequences of premature birth, affecting 5-15% of premature neonates with birth weights <1,500 grams. Many lines of evidence suggest a role for the dysregulation of enterocyte apoptosis in NEC pathogenesis. In addition to apoptosis, the roles of several inflammatory mediators such as platelet-activating factor, IL-8, TNFα and endotoxin have been shown to be pathogenic. Receptors for these ligands and downstream cellular signaling pathways, such as mitochondrial injury-induced caspase activation and NFĸB-mediated transcriptional regulation are thought to be involved in the mechanisms of mucosal injury in NEC. In this review, we attempt to summarize the role of enterocyte apoptosis in NEC along with an analysis of the connection between inflammatory signaling and apoptosis in this disease.