Abstract Title:

Aronia berry inhibits disruption of Caco-2 intestinal barrier function.

Abstract Source:

Arch Biochem Biophys. 2020 Jul 30 ;688:108409. Epub 2020 May 25. PMID: 32464089

Abstract Author(s):

Jonathan C Valdez, Junhyo Cho, Bradley W Bolling

Article Affiliation:

Jonathan C Valdez


The objective of this work was to determine how aronia berry polyphenols and its microbial catabolites improve intestinal barrier function. Caco-2 cells were cultured on transwell plates and allowed differentiate to form a model intestinal barrier, having baseline transepithelial electrical resistance (TEER) ≥ 300 Ω cm. Barrier function of differentiated Caco-2 cells was compromised by the addition of an inflammatory cocktail (IC: TNF-α, IL-1β, and IFN-γ to the basolateral media and lipopolysaccharide to the apical media). Polyphenol-rich aronia berry powder or individual polyphenols representative of parent compounds or catabolites were applied to the basolateral media concurrently with IC. TEER was determined subsequently by chopstick electrode or continuous analysis. Permeability was determined by application of 4 kDa FITC-dextran or Lucifer yellow. Expression of tight junction proteins was assessed by qRT-PCR analysis. Application of the ICto differentiated Caco-2 cells routinely reduced TEER by ~40% within 24 h. Individual polyphenols representative of parent compounds or phenolic microbial catabolites at 100 μM did not inhibit IC reduction of TEER in Caco-2 cells. Whole aronia berry powder inhibited loss of TEER by ~50% at 24 h after application of the IC. Furthermore 5 mg/mL of aronia berry powder prevented an IC-induced barrier permeability of FITC-dextran and Lucifer yellow. After 12 h of IC treatment, Caco-2 cells had increased claudin 1 (CLDN1) relative to the untreated control. Application of aronia berry powderinhibited CLDN1 and also increased expression of zonula ocludens-1 (ZO-1) after 12 h. In summary, aronia berry, but not its microbiota-derived catabolites improved intestinal barrier function in a cellular model of chronic colonic inflammation. In this case, improved barrier function was associated with modulation of tight junction expression.

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