Inflammatory signaling in NEC: Role of NF-κB, cytokines and other inflammatory mediators

Human milk exosomes and their microRNAs survive digestion in vitro and are taken up by human intestinal cells

“…Its identification in human milk exosomes expands its established role of modulating carbohydrate metabolism to a potential new domain of benefits in postnatal developmental programming. Furthermore, after exposing 293T cells to human recombinant TNF‐α for 6 h, overexpression of miR‐22‐3p was shown to significantly suppress NF‐κB activity , a key inflammatory signaling molecule that leads to necrotizing enterocolitis . This provides an additional molecular link to explain the preventive effect of breastfeeding on necrotizing enterocolitis.…”

Pathogenesis of NEC: Role of the innate and adaptive immune response

“…In particular, exaggerated TLR-4 signaling and LPS are thought to play a major role in the inflammatory signaling in NEC 177,178 . Of note, platelet activating factor (PAF) is also an important acute mediator in the pathogenesis of NEC, which is not only a chemokine that induces inflammatory signaling but also can increase expression of TLR-4 179-182 . TLR-9 may play a protective role 183-186 .…”

Case reports: necrotizing enterocolitis

“…In animal studies acetic and butyric acids have been shown to induce intestinal mucosal injury similar to NEC pathology in preterm infants [14,15] . Several groups have investigated the role of cytokines in the development, progression and severity of NEC [16][17][18] . Others have found that there is an alteration of intestinal bacterial colonization and lack of bacterial diversity in infants with NEC leading to a loss or suppression of healthy bacterial flora [19][20][21] .…”