Evidence map›Paper›PMID 38216767›Full record

ArticlePediatric surgery international2024

Human milk oligosaccharides promote intestinal epithelium regeneration independent of the microbiota during necrotizing enterocolitis.

Andrea Zito, Richard Y Wu, Bo Li, Steven R Botts, Mehrsa Feizi, Dorothy Lee, Carol Lee, Kathene C Johnson-Henry, Michael G Surette, Philip M Sherman and 1 more

Abstract read
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In one paragraph

Article in Pediatric surgery international, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

  1. Review
  2. Necrotizing Enterocolitis: What's New and What's Next?International journal of molecular sciences · 2025
    Review
  3. Article
  4. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Andrea ZitoTranslational Medicine Program, The Hospital for Sick Children, Toronto, ON, M5G 1X8, Canada.
Richard Y WuCell Biology Program, The Hospital for Sick Children, Toronto, ON, M5G 1X8, Canada.
Bo LiTranslational Medicine Program, The Hospital for Sick Children, Toronto, ON, M5G 1X8, Canada.
Steven R BottsCell Biology Program, The Hospital for Sick Children, Toronto, ON, M5G 1X8, Canada.
Mehrsa FeiziTranslational Medicine Program, The Hospital for Sick Children, Toronto, ON, M5G 1X8, Canada.
Dorothy LeeTranslational Medicine Program, The Hospital for Sick Children, Toronto, ON, M5G 1X8, Canada.
Carol LeeTranslational Medicine Program, The Hospital for Sick Children, Toronto, ON, M5G 1X8, Canada.
Kathene C Johnson-HenryCell Biology Program, The Hospital for Sick Children, Toronto, ON, M5G 1X8, Canada.
Michael G SuretteDepartment of Medicine, Faculty of Health Sciences, McMaster University, Hamilton, ON, L8S 4L8, Canada.
Philip M ShermanCell Biology Program, The Hospital for Sick Children, Toronto, ON, M5G 1X8, Canada.
Agostino PierroTranslational Medicine Program, The Hospital for Sick Children, Toronto, ON, M5G 1X8, Canada. agostino.pierro@sickkids.ca.

Funding

CIHR 353857CIHR MOP-89894
6 · The paper itself

Abstract

purposeNecrotizing enterocolitis (NEC) is a severe intestinal disease primarily affecting premature infants, marked by impaired epithelial regeneration. Breastfed infants are less susceptible to NEC than formula-fed ones, and human milk oligosaccharides (HMO) found in breast milk have prebiotic properties that can protect against NEC. However, it is unclear how HMOs influence intestinal epithelium regeneration in relation to the gut microbiota.

methodsBroad-spectrum antibiotics were administered to pregnant dams to reduce the microbiota in offspring. NEC was induced through administration of hyperosmolar formula, lipopolysaccharide, and hypoxia from postnatal days (p) 5-9. Intestinal epithelial organoids were derived from p9 mice. HMOs were isolated from human donor breast milk and then solubilized in the formula for each feed or culture media for organoids.

resultsHMOs did not alter the microbiota profile in the presence of a normal or reduced microbiota. In the reduced microbiota, HMO treatment decreased NEC intestinal injury, and increased proliferation and stem cell activity. Additionally, in the complete absence of the microbiota, HMOs stimulated intestinal organoid growth.

conclusionThis study demonstrates that HMOs promoted intestinal epithelial regeneration independent of the gut microbiota. These findings provide further insight into the various benefits HMOs may have in the protection against NEC.

Indexed as

Enterocolitis, NecrotizingInfant, Newborn, DiseasesMicrobiotaAnimalsFemaleHumansInfantInfant, NewbornIntestinal MucosaMiceMilk, HumanOligosaccharidesPregnancyRegenerationOligosaccharidesHuman milk oligosaccharidesIntestinal epithelial regenerationMicrobiotaNecrotizing enterocolitis

Identifiers

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Registered trials

None linked

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.