Metabolites of Latilactobacillus curvatus BYB3 and indole activate aryl hydrocarbon receptor to attenuate lipopolysaccharide-induced intestinal barrier dysfunction

Xing Wang1, Cheng Chung Yong1, Sejong Oh1,*
Author Information & Copyright
1Division of Animal Science, Chonnam National University, Gwangju 61186, Korea
*Corresponding Author: Sejong Oh, E-mail:

© Copyright 2022 Korean Society for Food Science of Animal Resources. This is an Open-Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Received: Jun 18, 2022 ; Revised: Aug 21, 2022 ; Accepted: Aug 27, 2022

Published Online: Sep 06, 2022


In this study aimed to investigate the effects of the metabolites of Latilactobacillus curvatus BYB3 and indole activate the AhR and increased the Tight junction protein in an in vitro model of intestinal inflammation. Western blotting analyses showed that the supernatants of Latilactobacillus curvatus BYB3, indole or metabolites of indole derivatives alleviated LPS simulated Caco-2 cell by upregulating the expression of TJ-associated proteins, namely zona occludens-1 (ZO-1), and claudin-1 (CLDN-1) and by suppressing nuclear factor-kappa B (NF-κB) signaling. Immunofluorescence images consistently revealed that LPS disrupts and reduces the expression of these TJ proteins, while the metabolites of L. curvatus BYB3 and indole reversed these alterations. Similar protective effects were observed on the intestinal barrier function upon examining transepithelial electrical resistance measurements. Metabolite analysis using high-performance liquid chromatography determined DL-indole-3-lactic acid (ILA), indole-3-acetamide (IAM) and indole, and the ILA and IAM concentrations were found to be 1.73±0.27mg/L and 0.51±0.39mg/L, respectively. Hence, our finding purpose of the attenuating damage caused by LPS to the intestinal epithelial barrier of the Caco-2 cells, because of enhancement of mRNA expression level of the CYP1A1 and AhR in response to the metabolites of L.curvatus BYB3 and indole.

Keywords: Latilactobacillus curvatus BYB3; aryl hydrocarbon receptor; Caco-2 cells; tight junction; lipopolysaccharide