Protective effects of taurine on growth performance and intestinal epithelial barrier function in weaned piglets challenged without or with lipopolysaccharide

2018 ◽  
Vol 58 (11) ◽  
pp. 2011 ◽  
Author(s):  
Zhiru Tang ◽  
Jinyan Liu ◽  
Zhihong Sun ◽  
Jinlong Li ◽  
Weizhong Sun ◽  
...  
Keyword(s):  
Growth Performance ◽  
Membrane Integrity ◽  
Intestinal Epithelial ◽  
Toll Like Receptor ◽  
Weaned Piglets ◽  
Intestinal Epithelial Barrier ◽  
Toll Like Receptor 4 ◽  
Epithelial Barrier Function ◽  
Mucosal Membrane ◽  
Small Intestinal

We evaluated whether weaned piglets were protected from bacterial endotoxins by placing the animals on a taurine-supplemented diet. A total of 40 weaned Landrace × Yorkshire piglets (5.75 ± 0.58 kg, weaned at 21 days) were allocated to four groups with 10 barrows per group, following a 2 × 2 factorial design with two inclusion levels of lipopolysaccharide (LPS) (no or one time peritoneal injection by the dose of 100 µg/kg bodyweight on Day 7 of the trial) and two inclusion levels of dietary taurine (no or 0.1% taurine in a basal diet in the whole trial). There was a significant interaction between LPS and taurine with regard to growth and small intestinal mucosal membrane integrity, morphology, immune parameters, and antioxidant capacity (P < 0.05). Feed conversion, daily weight gain, daily feed intake, villus height, and the villus to crypt ratio, vascular endothelial growth factor, regenerating islet-derived protein 3 gamma, trefoil factor-3, transforming growth factor β-1 expression, number of goblet cells and the least amount of claudin-1, occludin, zonula occludens-1, serum glutathione peroxidase, nitrogen oxide synthase, superoxide dismutase, peroxidase, and total antioxidant was lowest in LPS-challenged animals. Furthermore, animals in the LPS group had the highest serum diamine oxidase concentration, number of lymphocytes, concentrations of calprotectin, sIgA, toll-like receptor-4, mRNA levels of interleukin-1β, interleukin-8, toll-like receptor-4, and tumour necrosis factor-α (P < 0.05). These data suggested that the peritoneal injection administration of LPS decreased growth performance and disrupted small intestinal mucosal membrane integrity and triggered an inflammatory response in the small intestinal mucosal membrane. Dietary administration of taurine improved growth performance, increased small intestinal villus height, stimulated immune and antioxidant function and improved small intestinal mucosal membrane integrity in weaned piglets challenged without or with LPS (P < 0.05). The beneficial effects of taurine were likely due to decreased stimulation of the immune response to LPS and an improvement in intestinal epithelial barrier function. Dietary administration of taurine could prevent weaned piglets from intestinal damage by LPS of Gram-negative bacteria.

scholarly journals Retinoic Acid Facilitates Toll-Like Receptor 4 Expression to Improve Intestinal Barrier Function through Retinoic Acid Receptor Beta

2017 ◽  
Vol 42 (4) ◽  
pp. 1390-1406 ◽  
Author(s):  
Yingying Li ◽  
Yuan Gao ◽  
Ting Cui ◽  
Ting Yang ◽  
Lan Liu ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Barrier Function ◽  
Retinoic Acid Receptor ◽  
Epithelial Barrier ◽  
Intestinal Epithelial ◽  
Toll Like Receptor ◽  
Intestinal Epithelial Barrier ◽  
Epithelial Barrier Function ◽  
Expression Levels ◽  
Acid Receptor

Background/Aims: Vitamin A (VA) protects the intestinal epithelial barrier by improving cell migration and proliferation. Our previous studies demonstrated that VA deficiency (VAD) during pregnancy suppresses the systemic and mucosal immune responses in the intestines of offspring and that VA supplementation (VAS) during early life can increase immune cell counts. However, little is known about the mechanisms by which VA regulates intestinal epithelial barrier function. Methods: Caco-2 cells were treated with all-trans retinoic acid (ATRA) for 24 hours to determine the optimum ATRA concentration to which the cells in question respond. Caco-2 cells were infected with recombinant adenoviruses carrying retinoic acid receptor beta (Ad-RARβ) and small interfering RARβ(siRARβ) to assess the effects of RARβ signalling on the expression of specific proteins. A siTLR4 lentivirus was used to knockdown Toll-like receptor 4 (TLR4) in Caco-2 cells to determine its role in the protective effects of VA on the intestinal epithelial barrier, and experiments involving TLR4-knock-out mice were performed to verify the effect of TLR4. VA normal (VAN), VAD and VAS rat models were established to confirm that changes in RARβ, TLR4 and ZO-2 expression levels that occurred following decreases or increases in retinol concentrations in vivo, and the permeability of the Caco-2 cell monolayer, as well as that of the epithelial barrier of the rat intestine was detected by measuring transepithelial resistance (TER) or performing enzyme-linked immunosorbent assay (ELISA). Retinoic acid receptor (RAR), toll like receptor (TLR) and tight junction (TJ) mRNA and protein expression levels in Caco-2 cells and the colon monolayers in the rat and mouse models were measured by PCR and western blotting, respectively. Co-immunoprecipitation (co-IP) and immunofluorescence staining were performed to assess the interactions among RARβ, TLR4 and zonula occluden-2 (ZO-2) in Caco-2 cells, and chromatin immunoprecipitation (ChIP) assay was performed to assess the binding between RARβ and the TLR4 promoter sequence in Caco-2 cells. Results: In the present study, ATRA treatment not only increased the TER of the Caco-2 monolayer but also up-regulated the expression levels of RARβ, TLR4 and ZO-2 in Caco-2 cells. The expression levels of these three proteins were significantly decreased in the colonic epithelial monolayers of VAD rats compared with those of VAN rats and were significantly increased following VAS in the corresponding group compared with the control group. Furthermore, the above changes in TLR4 and ZO-2 expression levels were augmented or attenuated by Ad-RARβ or siRARβ infection, respectively, in Caco-2 cells. Interestingly, siTLR4 down-regulated ZO-2 expression but did not affect RARβ expression in Caco-2 cells, and in VAD mice the lack of TLR4 did not affect ZO-2 expression. We noted direct interactions between RARβ and TLR4, TLR4 and ZO-2 in Caco-2 cells, and ChIP assay showed that RARβ could bind to the TLR4 promoter but not the ZO-2 promoter in Caco-2 cells. Conclusion: Taken together, our results indicate that RARβ enhanced ZO-2 expression by regulating TLR4 to improve intestinal epithelial barrier function in Caco-2 cells, as well as in rat and mouse models, but not in humans.

The enteric nervous system as a regulator of intestinal epithelial barrier function in health and disease

2010 ◽  
Vol 4 (5) ◽  
pp. 637-651 ◽  
Author(s):  
Susanne A Snoek ◽  
Marleen I Verstege ◽  
Guy E Boeckxstaens ◽  
René M van den Wijngaard ◽  
Wouter J de Jonge
Keyword(s):  
Nervous System ◽  
Enteric Nervous System ◽  
Barrier Function ◽  
Epithelial Barrier ◽  
Intestinal Epithelial ◽  
Intestinal Epithelial Barrier ◽  
Epithelial Barrier Function ◽  
Health And Disease

scholarly journals JunD Represses Transcription and Translation of the Tight Junction Protein Zona Occludens-1 Modulating Intestinal Epithelial Barrier Function

2008 ◽  
Vol 19 (9) ◽  
pp. 3701-3712 ◽  
Author(s):  
Jie Chen ◽  
Lan Xiao ◽  
Jaladanki N. Rao ◽  
Tongtong Zou ◽  
Lan Liu ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Tight Junction ◽  
Barrier Function ◽  
Intestinal Epithelial Cells ◽  
Binding Protein ◽  
Mrna Translation ◽  
Epithelial Barrier ◽  
Intestinal Epithelial ◽  
Intestinal Epithelial Barrier ◽  
Epithelial Barrier Function

The AP-1 transcription factor JunD is highly expressed in intestinal epithelial cells, but its exact role in maintaining the integrity of intestinal epithelial barrier remains unknown. The tight junction (TJ) protein zonula occludens (ZO)-1 links the intracellular domain of TJ-transmembrane proteins occludin, claudins, and junctional adhesion molecules to many cytoplasmic proteins and the actin cytoskeleton and is crucial for assembly of the TJ complex. Here, we show that JunD negatively regulates expression of ZO-1 and is implicated in the regulation of intestinal epithelial barrier function. Increased JunD levels by ectopic overexpression of the junD gene or by depleting cellular polyamines repressed ZO-1 expression and increased epithelial paracellular permeability. JunD regulated ZO-1 expression at the levels of transcription and translation. Transcriptional repression of ZO-1 by JunD was mediated through cAMP response element-binding protein-binding site within its proximal region of the ZO-1-promoter, whereas induced JunD inhibited ZO-1 mRNA translation by enhancing the interaction of the ZO-1 3′-untranslated region with RNA-binding protein T cell-restricted intracellular antigen 1-related protein. These results indicate that JunD is a biological suppressor of ZO-1 expression in intestinal epithelial cells and plays a critical role in maintaining epithelial barrier function.

Sign in / Sign up

Export Citation Format

Share Document