Format

Send to

Choose Destination
Glycobiology. 2016 Jun;26(6):655-69. doi: 10.1093/glycob/cww002. Epub 2016 Jan 7.

Galectins are human milk glycan receptors.

Author information

1
Department of Biochemistry, School of Medicine, Emory University, Atlanta, GA, USA.
2
Department of Biochemistry, School of Medicine, Emory University, Atlanta, GA, USA Department of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, CLS 11087-3 Blackfan Circle, Boston, MA 02115, USA rcummin1@bidmc.harvard.edu.

Abstract

The biological recognition of human milk glycans (HMGs) is poorly understood. Because HMGs are rich in galactose we explored whether they might interact with human galectins, which bind galactose-containing glycans and are highly expressed in epithelial cells and other cell types. We screened a number of human galectins for their binding to HMGs on a shotgun glycan microarray consisting of 247 HMGs derived from human milk, as well as to a defined HMG microarray. Recombinant human galectins (hGal)-1, -3, -4, -7, -8 and -9 bound selectively to glycans, with each galectin recognizing a relatively unique binding motif; by contrast hGal-2 did not recognize HMGs, but did bind to the human blood group A Type 2 determinants on other microarrays. Unlike other galectins, hGal-7 preferentially bound to glycans expressing a terminal Type 1 (Galβ1-3GlcNAc) sequence, a motif that had eluded detection on non-HMG glycan microarrays. Interactions with HMGs were confirmed in a solution setting by isothermal titration microcalorimetry and hapten inhibition experiments. These results demonstrate that galectins selectively bind to HMGs and suggest the possibility that galectin-HMG interactions may play a role in infant immunity.

KEYWORDS:

galectins; glycan microarrays; glycan recognition; human milk glycans; shotgun glycomics

PMID:
26747425
PMCID:
PMC4847615
DOI:
10.1093/glycob/cww002
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Silverchair Information Systems Icon for PubMed Central
Loading ...
Support Center