Colonization by B. infantis EVC001 modulates enteric inflammation in exclusively breastfed infants

Bethany M. Henrick, Stephanie Chew, Giorgio Casaburi, Heather K. Brown, Steven A. Frese, You Zhou, Mark A. Underwood, Jennifer T. Smilowitz

Research output: Contribution to journalArticlepeer-review

21 Scopus citations


Background: Infant gut dysbiosis, often associated with low abundance of bifidobacteria, is linked to impaired immune development and inflammation—a risk factor for increased incidence of several childhood diseases. We investigated the impact of B. infantis EVC001 colonization on enteric inflammation in a subset of exclusively breastfed term infants from a larger clinical study. Methods: Stool samples (n = 120) were collected from infants randomly selected to receive either 1.8 × 1010 CFU B. infantis EVC001 daily for 21 days (EVC001) or breast milk alone (controls), starting at day 7 postnatal. The fecal microbiome was analyzed using 16S ribosomal RNA, proinflammatory cytokines using multiplexed immunoassay, and fecal calprotectin using ELISA at three time points: days 6 (Baseline), 40, and 60 postnatal. Results: Fecal calprotectin concentration negatively correlated with Bifidobacterium abundance (P < 0.0001; ρ = −0.72), and proinflammatory cytokines correlated with Clostridiaceae and Enterobacteriaceae, yet negatively correlated with Bifidobacteriaceae abundance. Proinflammatory cytokines were significantly lower in EVC001-fed infants on days 40 and 60 postnatally compared to baseline and compared to control infants. Conclusion: Our findings indicate that gut dysbiosis (absence of B. infantis) is associated with increased intestinal inflammation. Early addition of EVC001 to diet represents a novel strategy to prevent enteric inflammation during a critical developmental phase.

Original languageEnglish (US)
Pages (from-to)749-757
Number of pages9
JournalPediatric Research
Issue number6
StatePublished - Dec 1 2019

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health


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