ABSTRACT
The development of NEC reflects the interaction of colonizing microbes with the proinflammatory microenvironment of the intestinal mucosa seen during prematurity. While bacterial signaling via intestinal epithelial Toll-like receptor 4 (TLR4) plays a critical role in NEC development, the downstream responses to this cascade involve effector immune cells, which act upon the premature gut to cause the tissue destruction that characterizes NEC. This chapter explores the role of immune cells in NEC pathogenesis.
