Surviving patients with NEC are facing significant morbidity, including neurodevelopmental impairment, feeding problems, failure to thrive, dependence on parental nutrition, and short bowel syndrome. Although the pathogenesis of NEC remains elusive, a deregulated inflammatory response by the neonatal intestine to luminal bacteria is a unifying hypothesis. Intestinal epithelial injury is caused by different initiating events including intestinal ischemia, formula feeding, and colonization by opportunistic pathogens, leading to activation of the mucosal innate immune system and further damage of the epithelial barrier. Animal models as well as several clinical observations indicate that the intestine of preterm infants react with an excessive inflammatory response to luminal microbial stimuli as compared to the adult intestine. Correspondingly, NEC has been AbMole Benzyl alcohol associated with increased levels of AbMole Capromorelin tartrate pro-inflammatory cytokines in the inflamed intestine itself as well as in the blood flow. Animal models of NEC indicate that the release of pro-inflammatory cytokines promote intestinal ischemia and may under certain conditions cause septic shock in the absence of bacterial infection. Accordingly, interleukin -1 alpha levels correlate highly to intestinal inflammation and necrosis in a rabbit colitis model. IL-6 neutralization in mice after intestinal infection with Yersinia, caused a dramatic decrease in local and circulating IL1ra, suggesting that the pro-inflammatory IL-6 interplays with IL1 indirectly via IL-1ra. Anti-inflammatory cytokines are likely to play a protective role by inhibiting the inflammatory response. For example, intraperitoneal administration of IL-10 in an animal model of intestinal ischemia/reperfusion reduced local and systemic inflammation. A recent study by Emami and coworkers showed that IL-10 knockout mice developed more severe morphologic and histologic changes in a NEC model than wild type mice as evidenced by increased epithelial apoptosis, decreased junctional adhesion molecule-1 localization, and increased intestinal inducible nitric oxide synthase expression. Administration of exogenous IL-10 alleviated the mucosal injury. These animal model data show that different cytokines may have opposing effects. Thus, the course of the NEC disease depends finally on the relation of the different types of cytokines to each other. Such cytokine pattern studies have been extensively analyzed in adult patients with septic shock. But little is known about the ratio of pro-inflammatory to anti-inflammatory cytokines in preterm, very low birth weight infants suffering from NEC. Elevated concentrations of the pro-inflammatory cytokine IL-6 have been reported in infants with NEC. In addition, several studies have detected elevated IL-8 protein in NEC specimens. IL-8 levels are significantly higher in infants with NEC compared to other inflammatory conditions. We could recently show that the amount of IL-8 in the infant��s sera seems to correlate with disease extent. In addition, there are clinical studies reporting significantly elevated concentrations of the anti-inflammatory cytokine IL-10 in infants with NEC. The circumstance that all these study on different cytokines are measured in inconsistent study cohorts may withhold definitive conclusions which of the explored markers show the most promise for future clinical use.