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Abstract
Necrotizing enterocolitis (NEC) remains a leading cause of preterm infant mortality.
NEC is multifactorial and thought to be a consequence of intestinal immaturity, microbial
dysbiosis and an exuberant inflammatory response. Over the last decade, exaggerated
TLR4 activity in the immature intestine of preterm neonates emerged as an inciting
event preceding NEC. High TLR4 activity in epithelial cells results in the initiation
of an uncontrolled immune response and destruction of the mucosal barrier. We will
discuss the state of the science of the molecular mechanisms involved in TLR4-mediated
inflammation during NEC and the development of new therapeutic strategies to prevent
NEC.