scholarly journals Supplementation with yeast culture improves the integrity of intestinal tight junction proteins via NOD1/NF‐κB P65 pathway in weaned piglets and H2O2-challenged IPEC-J2 cells

2020 ◽  
Vol 72 ◽  
pp. 104058
Author(s):  
Shiqiong Wang ◽  
Suiliang Zhu ◽  
Jingjing Zhang ◽  
Haiyan Li ◽  
Dongji Yang ◽  
...  
2018 ◽  
Vol 20 (1) ◽  
pp. 20 ◽  
Author(s):  
Haiwei Liang ◽  
Zhaolai Dai ◽  
Jiao Kou ◽  
Kaiji Sun ◽  
Jingqing Chen ◽  
...  

l-Tryptophan (Trp) is known to play an important role in the health of the large intestine. However, a role of dietary Trp in the small-intestinal mucosal barrier and microbiota remains poorly understood. The present study was conducted with weaned piglets to address this issue. Postweaning piglets were fed for 4 weeks a corn- and soybean meal-based diet supplemented with 0 (Control), 0.1, 0.2, or 0.4% Trp. The small-intestinal microbiota and serum amino acids were analyzed by bacterial 16S rRNA gene-based high-throughput sequencing methods and high-performance liquid chromatography, respectively. The mRNA levels for genes involved in host defense and the abundances of tight-junction proteins in jejunum and duodenum were measured by real time-PCR and Western blot techniques, respectively. The concentrations of Trp in the serum of Trp-supplemented piglets increased in a dose-dependent manner. Compared with the control group, dietary supplementation with 0.2–0.4% Trp reduced the abundances of Clostridium sensu stricto and Streptococcus in the jejunum, increased the abundances of Lactobacillus and Clostridium XI (two species of bacteria that can metabolize Trp) in the jejunum, and augmented the concentrations of secretory immunoglobulin A (sIgA) as well as mRNA levels for porcine β-defensins 2 and 3 in jejunal tissues. Moreover, dietary Trp supplementation activated the mammalian target of rapamycin signaling and increased the abundances of tight-junction proteins (zonula occludens (ZO)-1, ZO-3, and claudin-1) in jejunum and duodenum. We suggested that Trp-metabolizing bacteria in the small intestine of weaned pigs primarily mediated the beneficial effects of dietary Trp on its mucosal integrity, health, and function.


2020 ◽  
Author(s):  
Wuying Lang ◽  
Haizhou Gong ◽  
Ruonan Li ◽  
Min Wu ◽  
Qianran Chu ◽  
...  

Abstract Background: Weaning causes stress syndrome in the newborns, while it can lead to many intestinal diseases. The aim of this study was to determine the dietary supplementation of β-carotene on growth performance, jejunal permeability and tight junction proteins in weaned piglets, and explore the underlying mechanisms by which β-carotene regulates tight junction proteins. The positive control group was fed sow's milk throughout the trial. The negative control group was weaned at d 21 without any supplementation. Two experimental groups of piglets were weaned at d 21 and fed 40 mg/kg or 80 mg/kg β-carotene-supplemented diets from d 14 to d 24, respectively. Blood and the jejunum were collected at d 24. Results: The results showed that β-carotene at 80 mg/kg increased initial and final body weight and average daily feed intake, improved the villus height at d 24 (p<0.05) but reduced crypt depth in weaned piglets at d 24 (p<0.05). Additionally, β-carotene protected intestinal morphology. Supplemental 80 mg/kg β-carotene reduced the concentrations of D-lactic acid and diamine oxidase in serum (p<0.05) but enhanced the mRNA expression of claudin-3, occludin (p<0.05), and zonula occludens protein-1(p>0.05) and the protein levels of claudin-3 (p<0.01), occludin (p<0.05), and zonula occludens protein-1 (p>0.05) in the jejunum at d 24. Using intestinal epithelial cells and a Rac1 inhibitor in vitro, we demonstrated that the β-carotene-induced higher tight junction proteins might depend on the Rac1 pathway. Conclusions: β-carotene improved growth performance and attenuated jejunal permeability and tight junction proteins in weaned piglets, suggesting that β-carotene at 80 mg/kg may be an effective way for keeping healthier intestine of weaning piglets due to weaning.


2018 ◽  
Vol 47 (4) ◽  
pp. 1617-1629 ◽  
Author(s):  
Wenqian Feng ◽  
Yancheng Wu ◽  
Guangxin Chen ◽  
Shoupeng Fu ◽  
Bai Li ◽  
...  

Background/Aims: Butyric acid plays an important role in maintaining intestinal health. Butyric acid has received special attention as a short-chain fatty acid, but its role in protecting the intestinal barrier is poorly characterized. Butyric acid not only provides energy for epithelial cells but also acts as a histone deacetylase inhibitor; it is also a natural ligand for G protein-coupled receptor 109A (GPR109A). A GPR109A analog was expressed in Sus scrofa and mediated the anti-inflammatory effects of beta-hydroxybutyric acid. This study investigated the effects of butyrate on growth performance, diarrhea symptoms, and tight junction protein levels in 21-day-old weaned piglets. We also studied the mechanism by which butyric acid regulates intestinal permeability. Methods: Twenty-four piglets that had been weaned at an age of 21 days were divided randomly into 2 equal groups: basal diet group and sodium butyrate + basal diet group. Diarrhea rate, growth performance during 3 weeks of feeding on these diets were observed, the lactulose-mannitol ratio in urine were detected by High Performance Liquid Chromatography, the expression levels of tight junction proteins in the intestinal tract and related signaling molecules, such as GPR109A and Akt, in the colon were examined by quantitative real-time PCR or western blot analyses on day 21. Caco-2 cells were used as a colon cell model and cultured with or without sodium butyrate to assess the expression of tight junction proteins and the activation of related signaling molecules. GPR109A-short hairpin RNA (shRNA) and specific antagonists of Akt and ERK1/2 were used as signaling pathway inhibitors to elucidate the mechanism by which butyric acid regulates the expression of tight junction proteins and the colonic epithelial barrier. Results: The sodium butyrate diet alleviated diarrhea symptoms and decreased intestinal permeability without affecting the growth of early weaned piglets. The expression levels of the tight junction proteins Claudin-3, Occludin, and zonula occludens 1 were up-regulated by sodium butyrate in the colon and Caco-2 cells. GPR109A knockdown using shRNA or blockade of the Akt signaling pathway in Caco-2 cells suppressed sodium butyrate-induced Claudin-3 expression. Conclusions: Sodium butyrate acts on the Akt signaling pathway to facilitate Claudin-3 expression in the colon in a GPR109A-dependent manner.


2005 ◽  
Vol 43 (05) ◽  
Author(s):  
Cs Páska ◽  
E Orbán ◽  
A Kiss ◽  
Zs Schaff ◽  
A Szijjártó ◽  
...  

2017 ◽  
Vol 95 (3) ◽  
pp. 1313 ◽  
Author(s):  
L. Zhang ◽  
L. F. Schütz ◽  
C. L. Robinson ◽  
M. L. Totty ◽  
L. J. Spicer

Lupus ◽  
2021 ◽  
Vol 30 (6) ◽  
pp. 926-936
Author(s):  
Georges Maalouly ◽  
Joelle Hajal ◽  
Charbel Noujeim ◽  
Michel Choueiry ◽  
Hussein Nassereddine ◽  
...  

Background Intestinal and hepatic manifestations of lupus seem to be underestimated in comparison to other major organ lesions. Although recent data point to gut-liver axis involvement in lupus, gut permeability dysfunction and liver inflammation need to be more investigated. Objective This study aims to assess fecal calprotectin, intestinal tight junction proteins and liver inflammation pathway in wild-type murine imiquimod- induced lupus. Methods C57BL/6 mice were topically treated on their right ears with 1.25 mg of 5% imiquimod cream, three times per week for six weeks. Fecal calprotectin was collected at day 0, 22 and 45. Renal, liver and intestinal pathology, as well as inflammatory markers, intestinal tight junction proteins, and E. coli protein in liver were assessed at sacrifice. Results At six weeks, lupus nephritis was confirmed on histopathology and NGAL and KIM-1 expression. Calprotectin rise started at day 22 and persists at day 45. Protein expression of Claudine, ZO-1 and occludin was significantly decreased. E. coli protein was significantly increased in liver with necro-inflammation and increased TLR4, TLR7, and pNFκB/NFκB liver expression. Conclusion This study is the first to demonstrate early fecal calprotectin increase and liver activation of TLR4- NFκB pathway in wild-type murine imiquimod-induced lupus.


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