Premium
Galacto‐oligosaccharides may directly enhance intestinal barrier function through the modulation of goblet cells
Author(s) -
Bhatia Shikha,
Prabhu P. Nagendra,
Benefiel Ann C.,
Miller Michael J.,
Chow JoMay,
Davis Steven R.,
Gaskins H. Rex
Publication year - 2015
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201400639
Subject(s) - goblet cell , mucin , western blot , chemistry , barrier function , secretion , microbiology and biotechnology , biology , biochemistry , gene , epithelium , genetics
Scope Here we have tested the hypothesis that prebiotic galacto‐oligosaccharides (GOS) may enhance mucosal barrier function through direct modulation of goblet cell function. Methods and results Human adenocarcinoma‐derived LS174T cells, which exhibit an intestinal goblet cell‐like phenotype, were used to examine the non‐prebiotic effects of GOS on goblet cell functions. LS174T cells were treated with GOS, and the expression of goblet cell secretory product genes mucin 2 ( MUC2) , trefoil factor 3 ( TFF3) , resistin‐like molecule beta ( RETNLB ) and the Golgi‐sulfotransferase genes, carbohydrate (N‐acetylglucosamine‐6‐O) sulfotransferase 5 ( CHST5) and galactose‐3‐O‐sulfotransferase 2 ( GAL3ST2 ), was determined by real‐time quantitative RT‐PCR. In addition, the abundance of CHST5, TFF3 and RETNLB was confirmed by Western blot analysis. Following treatment with GOS for 72 h, the expression of MUC2 was significantly upregulated 2–4‐fold, CHST5 and RETNLB , 5–7‐fold, and TFF3 2–4‐fold. Western blot analysis demonstrated increased abundance of RETNLB, TFF3 and CHST5. Addition of the Th2 cytokine IL‐13 along with GOS resulted in synergistic induction of RETNLB and CHST5 . IL‐8 secretion was not affected by GOS treatment, suggesting that the effects of GOS are not mediated through an inflammatory pathway. Conclusion Collectively, the data indicate that GOS may enhance mucosal barrier function through direct stimulation of intestinal goblet cells.