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Hyaluronan from human breast milk induces the expression of galectins 4 and 8 in intestinal epithelium (623.24)
Author(s) -
Kim Yeojung,
Petrey Aaron,
Kessler Sean,
Hill David,
Motte Carol
Publication year - 2014
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.28.1_supplement.623.24
Subject(s) - galectin , beta defensin , intestinal epithelium , biology , epithelium , in vivo , antimicrobial peptides , microbiology and biotechnology , cd44 , antimicrobial , downregulation and upregulation , defensin , immune system , glycan , tlr4 , salmonella , in vitro , immunology , bacteria , gene , glycoprotein , biochemistry , genetics
Human milk glycans play an important role in protecting infants from bacterial infections by providing antimicrobial molecules and promoting development of beneficial microbiota. We have shown that hyaluronan from human milk (milk HA), a milk glycan polymer, induces the expression of human beta defensin 2 (HBD2), an antimicrobial peptide in vitro and the mouse orthologue in vivo, through a Toll‐like receptor 4 (TLR4) and CD44 dependent manner . Importantly, milk HA reduces Salmonella infection of intestinal epithelial cells in vitro . We hypothesized that in addition to HBD2, additional antimicrobial molecules are regulated by HA. Our data suggest that Galectins 4 and 8 (Gal4 and 8) are regulated by milk HA. Gal4 and 8 mediate killing of blood group B expressing pathogenic E.coli and Gal8 plays a role in Salmonella killing. Our result shows that in epithelial cells, milk HA increases LGALS 4 and 8 mRNA expression levels ~4‐fold. Immunofluorescence histochemistry of intestinal tissue demonstrated that after milk HA treatment of mice, Gal 4 and 8 proteins are upregulated in and around luminal epithelium in vivo . In conclusion, HA treatment enhances the expression of galectins in intestinal epithelium and is a potential mechanism of protection from Salmonella infection. Grant Funding Source : Supported by NICHD