Fig. 3.

The role of TLR4 activation in the pathogenesis of NEC. Premature infants have elevated intestinal TLR4 expression compared to full-term infants. TLR4 becomes activated by colonizing Gram-negative microbes, resulting in significant mucosal inflammation, impaired epithelial repair and mucosal barrier breakdown, which permits bacterial translocation, further activating TLR4 on the intestinal mesenteric endothelium, and resulting in intestinal hypoperfusion and ischemia, leading to NEC. TLR4 activation can be inhibited by breast milk, probiotics or pharmacological inhibitors. Th17 cells, T-helper 17 cells; TLR4, toll-like receptor 4; Treg cells, regulatory T cells.