Dietary fibre-based SCFA mixtures promote both protection and repair of intestinal epithelial barrier function in a Caco-2 cell model.
Impaired gut barrier function plays an important role in the development of many diseases such as obesity, inflammatory bowel disease, and in HIV infection. Dietary fibres have been shown to improve intestinal barrier function through their fermentation products, short chain fatty acids (SCFAs), and the effects of individual SCFAs have been studied. Here, different SCFA mixtures representing possible compositions from fibre fermentation products were studied for protective and reparative effects on intestinal barrier function. The effect of fermentation products from four dietary fibres, i.e. resistant starch, fructooligosaccharides, and sorghum and corn arabinoxylan (varying in their branched structure) on barrier function was positively correlated with their SCFA concentration. Pure SCFA mixtures of various concentrations and compositions were tested using a Caco-2 cell model. SCFAs at a moderate concentration (40-80 mM) improved barrier function without causing damage to the monolayer. In a 40 mM SCFA mixture, the butyrate proportion at 20% and 50% showed both a protective and a reparative effect on the monolayer to disrupting agents (LPS/TNF-α) applied simultaneously or prior to the SCFA mixtures. Relating this result to dietary fibre selection, slow fermenting fibres that deliver appropriate concentrations of SCFAs to the epithelium with a high proportion of butyrate may improve barrier function.
Whistler Center for Carbohydrate Research, Department of Food Science, Purdue University, 745 Agriculture Mall Drive, West Lafayette, IN 47907, USA. hamakerb@purdue.edu.
Tingting
T
Chen
Whistler Center for Carbohydrate Research, Department of Food Science, Purdue University, 745 Agriculture Mall Drive, West Lafayette, IN 47907, USA. hamakerb@purdue.edu and Department of Food and Nutrition, Yeungnam University, Gyeongsan, Gyeongbuk 38541, Republic of Korea.
Choon Young
CY
Kim
Whistler Center for Carbohydrate Research, Department of Food Science, Purdue University, 745 Agriculture Mall Drive, West Lafayette, IN 47907, USA. hamakerb@purdue.edu.
Amandeep
A
Kaur
Whistler Center for Carbohydrate Research, Department of Food Science, Purdue University, 745 Agriculture Mall Drive, West Lafayette, IN 47907, USA. hamakerb@purdue.edu.
Lisa
L
Lamothe
Department of Internal Medicine, Division of Gastroenterology, Rush University Medical Center, Chicago, IL 60612, USA.
Maliha
M
Shaikh
Department of Internal Medicine, Division of Gastroenterology, Rush University Medical Center, Chicago, IL 60612, USA.
Ali
A
Keshavarzian
Whistler Center for Carbohydrate Research, Department of Food Science, Purdue University, 745 Agriculture Mall Drive, West Lafayette, IN 47907, USA. hamakerb@purdue.edu.
Bruce R
http://orcid.org/0000-0001-6591-942X
BR
Hamaker
D001419:Bacteria / Q000378:metabolism; D018938:Caco-2 Cells; D004043:Dietary Fiber / Q000378:metabolism*; D004847:Epithelial Cells / Q000378:metabolism* / Q000382:microbiology; D005232:Fatty Acids, Volatile / Q000378:metabolism*; D000069196:Gastrointestinal Microbiome; D006801:Humans; D007413:Intestinal Mucosa / Q000378:metabolism*; D007422:Intestines / Q000382:microbiology; D020011:Protective Agents / Q000378:metabolism*; D019108:Tight Junctions / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D004043:Dietary Fiber; D005232:Fatty Acids, Volatile; D020011:Protective Agents; D014409:Tumor Necrosis Factor-alpha