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Human Milk Oligosaccharides Increase Mucin Expression in Experimental Necrotizing Enterocolitis
Hosp Sick Children, Canada; Univ Toronto, Canada.
Hosp Sick Children, Canada.
Hosp Sick Children, Canada.
Hosp Sick Children, Canada.
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2019 (English)In: Molecular Nutrition & Food Research, ISSN 1613-4125, E-ISSN 1613-4133, Vol. 63, no 3, article id 1800658Article in journal (Refereed) Published
Abstract [en]

Scope Necrotizing enterocolitis (NEC) is a leading cause of morbidity and death in preterm infants, occurring more often in formula-fed than breastfed infants. Studies in both rats and humans show that human milk oligosaccharides (HMOs) lower the incidence of NEC, but the mechanism underlying such protection is currently unclear. Methods and Results By extracting HMOs from pooled human breastmilk, the impact of HMOs on the intestinal mucin levels in a murine model of NEC are investigated. To confirm the results, the findings are validated by exposing human intestinal epithelial cells and intestinal organoids to HMOs and evaluated for mucin expression. HMO-gavage to pups increases Muc2 levels and decreases intestinal permeability to macromolecular dextran. HMO-treated cells have increased Muc2 expression, decreased bacterial attachment and dextran permeability during challenge by enteric pathogens. To identify the mediators involved in HMO induction of mucins, it is demonstrated that HMOs directly induce the expression of chaperone proteins including protein disulfide isomerase (PDI). Suppression of PDI activity removes the protective effects of HMOs on barrier function in vitro as well as NEC protection in vivo. Conclusions Taken together, the results provide insights to the possible mechanisms by which HMOs protect the neonatal intestine through upregulation of mucins.

Place, publisher, year, edition, pages
WILEY , 2019. Vol. 63, no 3, article id 1800658
Keywords [en]
goblet cells; human milk oligosaccharides; intestinal epithelial barrier; mucus; necrotizing enterocolitis
National Category
Biochemistry and Molecular Biology
Identifiers
URN: urn:nbn:se:liu:diva-154570DOI: 10.1002/mnfr.201800658ISI: 000457651500007PubMedID: 30407734OAI: oai:DiVA.org:liu-154570DiVA, id: diva2:1290500
Note

Funding Agencies|Canadian Institutes of Health Research [CIHR MOP-89894, IOP-92890]; Vanier Graduate Student Award from the CIHR; Canada Research Chair in Gastrointestinal Disease

Available from: 2019-02-20 Created: 2019-02-20 Last updated: 2019-02-20

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Abrahamsson, ThomasLandberg, Eva
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Division of Children's and Women's healthFaculty of Medicine and Health SciencesDepartment of Paediatrics in LinköpingDivision of Cell BiologyDepartment of Clinical Chemistry
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