Contributors to Dysbiosis in Very-Low-Birth-Weight Infants

Abstract

The objective of this commentary was to analyze the causes and outcomes of gut microbiome dysbiosis in preterm infants who are born at very low birth weight (VLBW). The intrauterine development of VLBW infants is interrupted abruptly with preterm birth and followed by extrauterine, health-threatening conditions and sequelae. These infants develop intestinal microbial dysbiosis characterized by low diversity, an overall reduction in beneficial and/or commensal bacteria, and enrichment of opportunistic pathogens of the Gammaproteobacteria class. The origin of VLBW infant dysbiosis is not well understood and is likely the result of a combination of immaturity and medical care. We propose that these factors interact to produce inflammation in the gut, which further perpetuates dysbiosis. Understanding the sources of dysbiosis could result in interventions to reduce gut inflammation, decrease enteric pathology, and improve health outcomes for these vulnerable infants.

Keywords: dysbiosis; gut microbiome; health; prematurity.

Figure 1:

A non-inflamed (A) and inflamed (B) infant guts. A. In the non-inflamed infant gut, butyrate produced by commensal bacteria decreases oxygen levels in the gut lumen, lowering abundance of Enterobacteriaceae. Human milk promotes the growth of commensal bacteria via HMOs, while IgA in milk reduces Enterobacteriaceae growth. B. In the inflamed infant gut, oxygen in the gut lumen facilitates the growth of Enterobacteriaceae, which produces LPS and promotes inflammation. Antepartum factors, antibiotics, neonatal toxic stress, and neonatal enteral iron can also exacerbate the inflammatory milieu.