Metabolites of Latilactobacillus curvatus BYB3 and indole activate aryl hydrocarbon receptor to attenuate lipopolysaccharide-induced intestinal barrier dysfunction
Received: Jun 18, 2022 ; Revised: Aug 21, 2022 ; Accepted: Aug 27, 2022
Published Online: Sep 06, 2022
Abstract
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.