Preterm birth, defined as <37 weeks gestation age, is associated with an immature gastrointestinal tract, diminished gut barrier function, and underdeveloped immune function leading to increased morbidity and mortality compared to term infants.
Studies show that preterm infants are rapidly colonized by nosocomial, antibiotic-resistant bacteria associated with an increased risk of serious infection, negative impacts on neonatal growth and development.
To examine the effect of feeding B. infantis EVC001 to preterm infants, the current study, prospectively and longitudinally collected faecal samples from 77 infants born before 37 weeks and compared the gut microbial composition and development, as well as enteric inflammation profiles.
Infants were enrolled at Kaiser Orange County Anaheim and Irvine Neonatal Intensive Care Units, in California, and assigned to one of two distinct feeding protocols based on gestational age and weight at birth. One feeding protocol dictated daily feedings of B. infantis EVC001 (8 × 109 CFU) for infants born before 32 weeks and/or weighing less than 1500g at birth (n = 31) and a second feeding protocol was directed for premature infants born after 32 weeks and with a birth weight of over 1500g (“No probiotic”; n = 46).
Nurses collected fecal samples (brown circles) opportunistically throughout the patient's stay in the neonatal intensive care unit (NICU), aiming for two or more samples per week. Infants received human milk (maternal or donor) through 34 weeks corrected gestational age, as well as human milk-based human milk fortifier. After 34 weeks, infant formula was used in addition to human milk. Shotgun metagenome sequencing performed on samples collected from all 77 infants was used to classify the average community structure of the infant microbiome in all samples.
De-identified patient metadata were collected to compare the impact of other clinical interventions on the preterm infant gut microbiome and to account for known differences between the feeding cohorts.
The researchers conclude that EVC001-fed premature infants had increased colonisation of Bifidobacterium in their gut microbiome, an increase in genes conferring efficient utilisation of HMOs, significantly decreased overall abundance of antibiotic-resistant (bacterial) genomes (ARGs), and importantly, a decreased enteric inflammatory profile compared to premature infants not fed a probiotic, after accounting for other confounding clinical variables.
The report states: "We conclude that the use of B. infantis EVC001 in conjunction with human milk in premature infants provides a meaningful and low-risk approach to alter the gut microbiome composition and increase the abundance of a well-established infant gut symbiont that: increased human milk utilization; diminished enteric inflammation; and decreased the abundance of taxa associated with antibiotic-resistance and poor health outcomes.
"Together with human milk feeding, B. infantis EVC001 may help to mitigate microbiome-associated risk of morbidity and mortality in hospitalized infants. Future observational and/or controlled studies examining the impact of B. infantis EVC001 on preterm infant health outcomes are warranted."
Research background
A recent observational study comparing longitudinal faecal samples taken from preterm infants showed that supplementation with Bifidobacterium and Lactobacillus remodeled the gut microbiome, replicating a gut microbiome more closely resembling that of a term infant.
Distinct species-specific effects among Bifidobacterium are beginning to emerge that distinguish the ability among Bifidobacterium species to modulate host enteric inflammation and epithelial integrity from those that do not.
Beyond observational studies, extensive evidence has indicated a beneficial role of feeding Bifidobacterium longum subsp. infantis (B. infantis) to premature infants, with significant decreases in morbidity and mortality reported, including those from NEC.
In animal models, B. infantis supplementation was effective at reducing NEC injury scores and minimising intestinal inflammation.
Establishing B. infantis abundance in the infant gut has been shown to restore important ecosystem services of the microbiome that are beneficial to infant health, particularly, the efficient fermentation of human milk oligosaccharides (HMOs) into host-accessible organic acids (e.g., acetate and lactate) helps reduce degradation of gastrointestinal mucin, and results in significant reductions of bacterial populations with pathogenic potential.
Moreover, when B. infantis is compared directly to other probiotic bacteria, including Bifidobacterium animalis subsp. lactis (B. lactis), it showed superior ability to colonize the premature infant gut.
Source: Frontiers in Pediatrics
Henrick. B. M., et al
"Impact of Probiotic B. infantis EVC001 Feeding in Premature Infants on the Gut Microbiome, Nosocomially Acquired Antibiotic Resistance, and Enteric Inflammation"