Gut Microbiome–Brain Axis as an Explanation for the Risk of Poor Neurodevelopment Outcome in Preterm Infants with Necrotizing Enterocolitis

Abstract

Necrotizing Enterocolitis (NEC) is characterized by an inflammation of intestinal tissue that primarily affects premature infants. It is the most common and devastating gastrointestinal morbidity of prematurity, but beyond intestinal morbidity, this condition has also been associated with an increased risk of neurodevelopmental delays that persist beyond infancy. Prematurity, enteral feeding, bacterial colonization, and prolonged exposure to antibiotics are all risk factors that predispose preterm infants to NEC. Interestingly, these factors are all also associated with the gut microbiome. However, whether or not there is a connection between the microbiome and the risk of neurodevelopmental delays in infants after NEC is still an emerging area of research. Furthermore, how microbes in the gut could impact a distant organ such as the brain is also poorly understood. In this review, we discuss the current understanding of NEC and the role of the gut microbiome–brain axis in neurodevelopmental outcomes after NEC. Understanding the potential role of the microbiome in neurodevelopmental outcomes is important as the microbiome is modifiable and thus offers the hope of improved therapeutic options. We highlight the progress and limitations in this field. Insights into the gut microbiome–brain axis may offer potential therapeutic approaches to improve the long-term outcomes of premature infants.

Potential Epigenetic Effects of Human Milk on Infants’ Neurodevelopment

“…There is evidence that the gut microbiome during early life contributes to the establishment of epigenetic modifications and it is also associated with brain development and neurodevelopment [ 113 , 114 , 115 ]. The colonization of the infant’s intestine after birth, influenced by maternal flora, delivery method, early skin-to-skin contact, and neonatal diet, results in specific epigenetic patterns that can influence the protective function of the gut mucosa against future insults [ 116 ].…”