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Human milk oligosaccharides alter the intestinal epithelial cell surface glycome: A proof‐of‐principle
Author(s) -
Straubinger Kathrin,
Niuevo Milady,
Bode Lars
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.206.2
Subject(s) - glycome , glycan , mannose , in vitro , glycomics , biology , biochemistry , cell , in vivo , chemistry , glycoprotein , genetics
Human Milk Oligosaccharides (HMO) are thought to benefit the breast‐fed infant. However, the exact underlying molecular mechanisms remain unknown. Prebiotic, anti‐adhesive and immunomodulating mechanisms have been postulated. Here, we propose an additional mechanism: Intestinal Glycome‐modification. Pathogen attachment to the intestine is often the initial step of infectious diseases and is mediated by pathogen lectins that bind to the host's intestinal epithelial cell surface glycans. We hypothesize that HMO alter the expression of these cell surface glycans, and thus interfere with host‐microbial interactions. Caco‐2 cell membrane proteins were isolated, N‐glycans released by PNGaseF digest and analyzed by mass spectrometry. Isotopically labeled N‐glycans were used as internal standard. While the relative distribution of high‐mannose N‐glycans was not altered, HMO increased the amount of all individual high‐mannose N‐glycans by 1.8–2.0‐fold. Analysis of Caco‐2 cell mRNA with the glycoV4 oligonucleotide gene array showed that HMO induce differential expression of glycan related genes. Galactooligosaccharides (GOS), currently added to infant formula to mimic HMO, had no effect. In conclusion, our in vitro results establish the proof‐of‐principle that HMO have glycome‐modifying effects. Whether these in vitro results translate to in vivo needs further investigation.