Role of human milk oligosaccharides in Group B Streptococcus colonisation

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Title: Role of human milk oligosaccharides in Group B Streptococcus colonisation
Authors: Andreas, NJ
Al-Khalidi, A
Jaiteh, M
Clarke, E
Hyde, M
Modi, N
Holmes, E
Kampmann, B
Mehring-Le Doare, K
Item Type: Journal Article
Abstract: Group B Streptococcus (GBS) infection is a major cause of morbidity and mortality in infants. The major risk factor for GBS disease is maternal and subsequent infant colonisation. It is unknown whether human milk oligosaccharides (HMOs) protect against GBS colonisation. HMO production is genetically determined and linked to the Lewis antigen system. We aimed to investigate the association between HMOs and infant GBS colonisation between birth and postnatal day 90. Rectovaginal swabs were collected at delivery, as well as colostrum/breast milk, infant nasopharyngeal and rectal swabs at birth, 6 days and days 60–89 postpartum from 183 Gambian mother/infant pairs. GBS colonisation and serotypes were determined using culture and PCR. 1H nuclear magnetic resonance spectroscopy was used to characterise the mother’s Lewis status and HMO profile in breast milk. Mothers who were Lewis-positive were significantly less likely to be colonised by GBS (X2=12.50, P<0.001). Infants of Lewis-positive mothers were less likely GBS colonised at birth (X2=4.88 P=0.03) and more likely to clear colonisation between birth and days 60–89 than infants born to Lewis-negative women (P=0.05). There was no association between Secretor status and GBS colonisation. In vitro work revealed that lacto-N-difucohexaose I (LNDFHI) correlated with a reduction in the growth of GBS. Our results suggest that HMO such as LNDFHI may be a useful adjunct in reducing maternal and infant colonisation and hence invasive GBS disease. Secretor status offers utility as a stratification variable in GBS clinical trials.
Issue Date: 26-Aug-2016
Date of Acceptance: 29-Jun-2016
ISSN: 2050-0068
Publisher: Nature Publishing Group
Journal / Book Title: Clinical and Translational Immunology
Volume: 5
Copyright Statement: This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://
Sponsor/Funder: Wellcome Trust
Thrasher Research Fund
Funder's Grant Number: 104482/Z/14/Z
Publication Status: Published
Article Number: e99
Appears in Collections:Division of Surgery
Department of Medicine
Faculty of Medicine

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