Editors' ChoicePEDIATRICS

Growing good bugs with mom’s milk

See allHide authors and affiliations

Science Translational Medicine  18 Oct 2017:
Vol. 9, Issue 412, eaap8172
DOI: 10.1126/scitranslmed.aap8172


A strain of Propionibacterium found in the gut of breast milk–fed infants confers immune protective effects that may mitigate risk of necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) is a highly morbid disease primarily afflicting premature infants. While its pathogenesis remains poorly understood, gut microbial colonization in the setting of compromised mucosal defense is thought to play a central role. Feeding with human breast milk is known to reduce risk of NEC, but exactly how breast milk confers protection is less clear. Colliou et al. report evidence that implicates breast milk–induced growth of Propionibacterium in the gut of preterm infants.

Using comprehensive gut microbiome profiling of breast milk–fed (BMF) and formula-fed (FF) preterm infants, the authors demonstrated increased bacterial diversity in BMF infants. To evaluate the functional significance of this diet-associated microbiota shift, they transferred fecal microbial communities from BMF or FF infants into germ-free mice. Mice receiving the BMF microbiota had increased numbers of colonic T helper 17 (TH17) cells and regulatory T (Treg) cells, two populations implicated in mucosal barrier repair and control of inflammation.

So what is the protective factor unique to the BMF microbiota? Propionibacterium was one bacterial genus increased in BMF vs. FF infants. The authors isolated a strain of Propionibacterium, called P. UF1, from BMF feces and discovered that transferring this strain into germ-free mice, either alone or in combination with the FF microbiota, was sufficient to recapitulate the protective immune effects conferred by the BMF microbiota and also to reduce inflammation induced by the pathogen Listeria monocyotogenes. Probing further, the authors found that P. UF1-induced TH17 cells recognized a protein in the bacterial surface layer, dihydrolipoamide acetyltransferase (DlaT). Furthermore, deleting DlaT from P. UF1 prevented the bacterium’s TH17-promoting effects.

Lastly, the authors explored the relevance of P. UF1 to NEC. In a model of neonatal colitis, pups born to mothers receiving P. UF1 during pregnancy had increased colonic TH17 and Treg cells and were protected from weight loss and death following NEC-like injury. These findings provide new mechanistic insight into the protective effects of human breast milk in preterm infants and highlight the promise of pursuing probiotic or molecular therapies to reduce NEC risk in infants for whom breast milk feeding is not possible.

Highlighted Article

View Abstract

Navigate This Article