Inhibition of Attachment of Streptococcus pneumoniae and Haemophilus influenzae by Human Milk and Receptor Oligosaccharides

Human milk inhibited the attachment of Streptococcus pneumoniae and Haemophilus influenzae to human pharyngeal or buccal epithelial cells. Infant formulas and cow and buffalo milk showed a lower inhibitory activity against pneumococci and enhanced the adhesion of H. influenzae. The antiadhesive effe...

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Published in:The Journal of infectious diseases Vol. 153; no. 2; pp. 232 - 237
Main Authors: Andersson, Bengt, Porras, Oscar, Hanson, Lars Å., Lagergård, Teresa, Svanborg-Edén, Catharina
Format: Journal Article
Language:English
Published: Chicago, IL The University of Chicago Press 01-02-1986
University of Chicago Press
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Summary:Human milk inhibited the attachment of Streptococcus pneumoniae and Haemophilus influenzae to human pharyngeal or buccal epithelial cells. Infant formulas and cow and buffalo milk showed a lower inhibitory activity against pneumococci and enhanced the adhesion of H. influenzae. The antiadhesive effect against S. pneumoniae was found in both the high- and the low-molecular-weight fractions of milk. The inhibitory activity in the high-molecular-weight fraction was independent of specific antibody content; it was present after immunoadsorption and in the milk from IgA-deficient women. The inhibitory activity in the low-molecular-weight fraction was in part explained by the content of oligosaccharides corresponding to the carbohydrate moieties of the neolactoseries of glycolipids, which have previously been shown to act as receptors for attaching pneumococci. The antiadhesive activity against H. influenzae was restricted to the high-molecular-weight fraction of the milk and was unaffected by immunoadsorption. Milk may protect against otitis by reducing colonization.
Bibliography:Please address requests for reprints to Dr. Bengt Andersson, Department of Clinical Immunology, University of Goteborg, Guldhedsgatan 10, 413 46, Göteborg, Sweden.
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ISSN:0022-1899
1537-6613
DOI:10.1093/infdis/153.2.232