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Necrotising enterolcolitis (NEC) is a common and devastating disease in preterm infants.1 The prevention of NEC has become a high research priority. NEC is precipitated by the exposure of the immature intestine to bacteria after birth. Studies in animal models and xenografts suggest that the preterm infant mounts an excessive inflammatory response to luminal bacteria.2–4 In the term infant, the intestine adapts to luminal microbes by downregulating the immune system, whereas, in the preterm infant, it does not. Intestinal epithelial cell toll-like receptor (TLR)4 responses appear to be much more active in the preterm intestine than in the term intestine.3 ,4 Intestinal epithelial TLR4 activation, driven by exposure to luminal Gram-negative bacteria, leads to increased mucosal injury through accelerated enterocyte apoptosis as well as reduced healing through impaired intestinal restitution and proliferation.3 Mice deficient in TLR4 show reduced severity in models of NEC. Apoptosis of epithelial cells is seen in histologic specimens collected at the time of small bowel resection in patients with NEC. Apoptosis usually precedes other signs of tissue damage. Animal models of NEC also demonstrate epithelial apoptosis. Clinical trials with breast milk feeding and probiotics (including Lactobacillus acidophilus and Bifidobacterium bifidum) have shown efficacy in preventing NEC.5 ,6
Zani et al7 demonstrate that amniotic fluid stem (AFS) cells given intraperitoneally improve survival and enhance repair of damaged intestine in a rat model of NEC. …
Competing interests None.
Provenance and peer review Commissioned; internally peer reviewed.
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