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Volume 18
Issue 10
10.3390/toxins18100451
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This is an early access version, the complete PDF, HTML, and XML versions will be available soon.
Article

Aryl Hydrocarbon Receptor Deficiency Impairs Intestinal Barrier Development, While 2′-Fucosyllactose Reduces Paracellular Permeability in Caco-2 Cells

by
Avra Melina Madella
1,
Carlon Catharina Emma van Gerven
1,
Elena Sendino Garví
1,
Jeroen van Bergenhenegouwen
2,
Johan Garssen
1,2,
Rosalinde Masereeuw
1 and
Saskia Adriana Overbeek
2,*
1
Division of Pharmacology, Utrecht Institute for Pharmaceutical Sciences, Utrecht University, 3584 CG Utrecht, The Netherlands
2
Danone Nutricia Research, 3584 CT Utrecht, The Netherlands
*
Author to whom correspondence should be addressed.
Toxins 2026, 18(10), 451; https://doi.org/10.3390/toxins18100451
Submission received: 31 August 2026 / Revised: 12 October 2026 / Accepted: 13 October 2026 / Published: 15 October 2026
(This article belongs to the Special Issue New Insights in Uremic Toxins and Toxin-Related Outcomes in Chronic Kidney Disease)
Versions Notes

Abstract

Chronic kidney disease (CKD) is increasingly linked to intestinal barrier dysfunction, which contributes to systemic inflammation and disease progression. We investigated whether 2′-fucosyllactose (2′-FL), a human milk oligosaccharide, could modulate intestinal epithelial barrier function under uremic toxin exposure and examined the role of the aryl hydrocarbon receptor (AhR). Using wild-type (WT) and AhR knockout (AhR KO) Caco-2 cell lines, we assessed barrier function and cellular responses through transepithelial electrical resistance (TEER), paracellular permeability (Papp), tight junction (TJ) gene expression, AhR target gene activation, and metabolic assays. AhR deficiency impaired epithelial maturation, confirming its role in barrier development. Short-term exposure to uremic toxins (UTs) did not significantly affect TEER or paracellular permeability under the conditions tested. However, 2′-FL reduced paracellular permeability in both WT and AhR KO cells in the presence of FCS. These effects occurred without changes in TJ gene expression, indicating mechanisms beyond transcriptional regulation. AhR target genes were not induced by UTs, suggesting limited receptor activation, and metabolic activity was unaffected. Overall, 2′-FL reduced paracellular permeability under selected experimental conditions, while the impaired barrier development observed in AhR-deficient cells supports a role for AhR in intestinal epithelial barrier development.
Keywords: 2′-FL; AhR; barrier dysfunction; human milk oligosaccharides; intestinal homeostasis; uremia 2′-FL; AhR; barrier dysfunction; human milk oligosaccharides; intestinal homeostasis; uremia

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MDPI and ACS Style

Madella, A.M.; van Gerven, C.C.E.; Sendino Garví, E.; van Bergenhenegouwen, J.; Garssen, J.; Masereeuw, R.; Overbeek, S.A. Aryl Hydrocarbon Receptor Deficiency Impairs Intestinal Barrier Development, While 2′-Fucosyllactose Reduces Paracellular Permeability in Caco-2 Cells. Toxins 2026, 18, 451. https://doi.org/10.3390/toxins18100451

AMA Style

Madella AM, van Gerven CCE, Sendino Garví E, van Bergenhenegouwen J, Garssen J, Masereeuw R, Overbeek SA. Aryl Hydrocarbon Receptor Deficiency Impairs Intestinal Barrier Development, While 2′-Fucosyllactose Reduces Paracellular Permeability in Caco-2 Cells. Toxins. 2026; 18(10):451. https://doi.org/10.3390/toxins18100451

Chicago/Turabian Style

Madella, Avra Melina, Carlon Catharina Emma van Gerven, Elena Sendino Garví, Jeroen van Bergenhenegouwen, Johan Garssen, Rosalinde Masereeuw, and Saskia Adriana Overbeek. 2026. "Aryl Hydrocarbon Receptor Deficiency Impairs Intestinal Barrier Development, While 2′-Fucosyllactose Reduces Paracellular Permeability in Caco-2 Cells" Toxins 18, no. 10: 451. https://doi.org/10.3390/toxins18100451

APA Style

Madella, A. M., van Gerven, C. C. E., Sendino Garví, E., van Bergenhenegouwen, J., Garssen, J., Masereeuw, R., & Overbeek, S. A. (2026). Aryl Hydrocarbon Receptor Deficiency Impairs Intestinal Barrier Development, While 2′-Fucosyllactose Reduces Paracellular Permeability in Caco-2 Cells. Toxins, 18(10), 451. https://doi.org/10.3390/toxins18100451

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