Vitamin D Reverses Disruption of Gut Epithelial Barrier Function Caused by .

Int J Mol Sci

Nutritional Medicine/Clinical Physiology, Medical Department, Division of Gastroenterology, Infectious Diseases, Rheumatology, Charité-Universitätsmedizin Berlin, 12203 Berlin, Germany.

Published: August 2021

Infections by the zoonotic foodborne bacterium () are among the most frequent causes of bacterial gastroenteritis worldwide. The aim was to evaluate the relationship between epithelial barrier disruption, mucosal immune activation, and vitamin D (VD) treatment during infection, using intestinal epithelial cells and mouse models focused on the interaction of with the VD signaling pathway and VD treatment to improve -induced barrier dysfunction. Our RNA-Seq data from campylobacteriosis patients demonstrate inhibition of VD receptor (VDR) downstream targets, consistent with suppression of immune function. Barrier-preserving effects of VD addition were identified in -infected epithelial cells and IL-10 mice. Furthermore, interference of with the VDR pathway was shown via VDR/retinoid X receptor (RXR) interaction. Paracellular leakiness of infected epithelia correlated with tight junction (TJ) protein redistribution off the TJ domain and apoptosis induction. Supplementation with VD reversed barrier impairment and prevented inhibition of the VDR pathway, as shown by restoration of transepithelial electrical resistance and fluorescein (332 Da) permeability. We conclude that VD treatment restores gut epithelial barrier functionality and decreases bacterial transmigration and might, therefore, be a promising compound for treatment in humans and animals.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8396270PMC
http://dx.doi.org/10.3390/ijms22168872DOI Listing

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