ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2023
Human milk oligosaccharides reduce necrotizing enterocolitis-induced neuroinflammation and cognitive impairment in mice.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 22 citations in OpenAlex.
- 2'-Fucosyllactose Effects on Preterm Growth, Tolerance, and Neurobehavior: A Double-Blind, Randomized, Placebo-Controlled Pilot.Nutrients · 2026Trial
- Nutritional regulation of gut-brain immune crosstalk across the lifespan.Gut microbes · 2026Review
- The potential of human milk oligosaccharides in ameliorating traumatic brain injury-induced cognitive impairment in mice.Future science OA · 2026Article
- The central function and specific molecular mechanisms of the TLR4 pathway underlying impaired intestinal barrier in necrotizing enterocolitis.Biochemistry and biophysics reports · 2026Review
- Intestinal Fucosylation: A Key Regulatory Hub in Homeostasis and Disease Pathogenesis.Biomolecules · 2026Review
- [Berberine attenuates necrotizing enterocolitis-associated brain injury via the TLR4/MyD88/NF-κB/NLRP3 pathway].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2026Article
- Shaping of the Infant Gut Microbiome by Milk Oligosaccharides.Annual review of biochemistry · 2026Review
- Necrotizing enterocolitis.Nature reviews. Disease primers · 2026Review
- Neuroprotective Effects of Desert Milk Exosomes in LPS-Induced Cognitive Decline: Role of Microglial M2 Polarization and AMPK Signaling.Nutrients · 2026Article
- Pathogenesis of necrotizing enterocolitis: mechanisms and mediators.World journal of pediatric surgery · 2026Review
- Neurodevelopmental impairment in infants with necrotizing enterocolitis: a comprehensive review of mechanisms, outcomes, and emerging strategies.World journal of pediatric surgery · 2026Review
- Supplementation with 2'-fucosyllactose, a prebiotic human milk oligosaccharide (HMO), in a magnesium-containing medical food reduces chemotherapy-induced mucositis in Wistar rats.Frontiers in nutrition · 2026Article
- Gastrointestinal Journey of Human Milk Oligosaccharides: From Breastfeeding Origins to Functional Roles in Adults.Microorganisms · 2025Review
- Necrotizing enterocolitis: specific human milk oligosaccharides prevent enteric glia loss and hypomotility.Pediatric research · 2025Article
- Necrotizing Enterocolitis: A Comprehensive Review on Toll-like Receptor 4-Mediated Pathophysiology, Clinical, and Therapeutic Insights.Biomedicines · 2025Review
- REGγ-mediated Barrier Disruption and NF-κB Activation Aggravates Intestinal Inflammation in Necrotizing Enterocolitis.Inflammation · 2025Article
- Antioxidant and Inflammation-Attenuating Ability of Human Milk, Infant Formulas and Their Oligosaccharides.Foods (Basel, Switzerland) · 2025Article
- Recent advances in the science of human milk oligosaccharides.BBA advances · 2025Article
- Human milk oligosaccharides: bridging the gap in intestinal microbiota between mothers and infants.Frontiers in cellular and infection microbiology · 2024Review
- Superior performance of biofilm versus planktonic Limosilactobacillus reuteri in protection of the intestines and brain in a piglet model of necrotizing enterocolitis.Scientific reports · 2023Article
Corrections and comments
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Authors and funding
23 authors at 2 institutions in 1 country.
Funding
Abstract
Necrotizing enterocolitis (NEC) is the leading cause of morbidity and mortality in premature infants. One of the most devastating complications of NEC is the development of NEC-induced brain injury, which manifests as impaired cognition that persists beyond infancy and which represents a proinflammatory activation of the gut-brain axis. Given that oral administration of the human milk oligosaccharides (HMOs) 2'-fucosyllactose (2'-FL) and 6'-sialyslactose (6'-SL) significantly reduced intestinal inflammation in mice, we hypothesized that oral administration of these HMOs would reduce NEC-induced brain injury and sought to determine the mechanisms involved. We now show that the administration of either 2'-FL or 6'-SL significantly attenuated NEC-induced brain injury, reversed myelin loss in the corpus callosum and midbrain of newborn mice, and prevented the impaired cognition observed in mice with NEC-induced brain injury. In seeking to define the mechanisms involved, 2'-FL or 6'-SL administration resulted in a restoration of the blood-brain barrier in newborn mice and also had a direct anti-inflammatory effect on the brain as revealed through the study of brain organoids. Metabolites of 2'-FL were detected in the infant mouse brain by nuclear magnetic resonance (NMR), whereas intact 2'-FL was not. Strikingly, the beneficial effects of 2'-FL or 6'-SL against NEC-induced brain injury required the release of the neurotrophic factor brain-derived neurotrophic factor (BDNF), as mice lacking BDNF were not protected by these HMOs from the development of NEC-induced brain injury. Taken in aggregate, these findings reveal that the HMOs 2'-FL and 6'-SL interrupt the gut-brain inflammatory axis and reduce the risk of NEC-induced brain injury.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.