Abstract
Prebiotics are non-digestible oligosaccharides that promote the growth of beneficial gut microbes, but it is unclear whether they also have direct effects on the intestinal mucosal barrier. Here we demonstrate two commercial prebiotics, inulin and short-chain fructo-oligosaccharide (scFOS), when applied onto intestinal epithelia in the absence of microbes, directly promote barrier integrity to prevent pathogen-induced barrier disruptions. We further show that these effects involve the induction of select tight junction (TJ) proteins through a protein kinase C (PKC) δ-dependent mechanism. These results suggest that in the absence of microbiota, prebiotics can directly exert barrier protective effects by activating host cell signaling in the intestinal epithelium, which represents a novel alternative mechanism of action of prebiotics.
Highlights
Prebiotics are non-digestible oligosaccharides that promote the growth of beneficial gut microbes, but it is unclear whether they have direct effects on the intestinal mucosal barrier
It is generally recognized that prebiotics affect human health by altering the gut microbiota[5], much less is known about the extent of direct effects on the host mucosal surface[2]
We tested this possibility to provide the first evidence for a direct mechanism whereby prebiotics, agents believed to be mostly inert to the host, activate the PKCδsignal transduction pathway to regulate tight junction (TJ) integrity and mitigate the deleterious effects of Escherichia coli O157:H7 (EHEC)
Summary
Prebiotics are non-digestible oligosaccharides that promote the growth of beneficial gut microbes, but it is unclear whether they have direct effects on the intestinal mucosal barrier. We measured the transepithelial electrical resistance (TER) of Caco-2Bbe[1] monolayers in response to inulin and scFOS with or without EHEC challenge. Similar to Caco-2Bbe[1] cells, pre-incubation of organoids with either inulin or scFOS significantly increased TER during EHEC challenge (Fig. 1d) and prevented the EHEC-mediated increase in FITC dextran permeability (Fig. 1e).
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