scholarly journals Galli gigeriae endothelium corneum: its intestinal barrier protective activity in vitro and chemical composition

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Shanshan Li ◽  
Meng Zheng ◽  
Zhentang Zhang ◽  
Hengying Peng ◽  
Wenling Dai ◽  
...  
Keyword(s):  
Chemical Composition ◽  
Mrna Expression ◽  
Barrier Function ◽  
Intestinal Barrier ◽  
Raw264.7 Cells ◽  
Intestinal Barrier Function ◽  
Dependent Manner ◽  
Chemical Profile ◽  
Tnf Α ◽  
Junction Protein

Abstract Background Galli gigeriae endothelium corneum (GGEC) has been effectively used for centuries for the treatment of functional dyspepsia (FD) in clinical practice in Asian countries. However, its potential mechanism and chemical composition remains undertermined. Methods In this study, the chemical profile of GGEC ethyl acetate extract (EAE) was evaluated by HPLC-Q-TOF–MS/MS. The effects of EAE on intestinal barrier function and inflammation were investigated in IEC-6 cells and RAW264.7 cells. Results The results showed that 33 compounds were tentatively identified, including 12 soy isoflavones, 7 bile acids for the first time in EAE. EAE significantly reinforced intestinal barrier function via increasing the tight junction protein levels of ZO-1 and Occludin, reducing the mRNA expression levels of interleukin (IL)-1β and IL-6 in tumor necrosis factor alpha (TNF-α)-challenged IEC-6 cells. The scratch wound assay showed that EAE accelerated wound healing of IEC-6 cells. EAE evidently reduced the level of NO in a dose-dependent manner with an IC50 value of 18.12 μg/mL, and the mRNA expression of TNF-α, IL-1β, IL-6, iNOS and COX-2 in LPS-treated RAW264.7 cells. Conclusion This study revealed the intestinal barrier protective effects and chemical profile of GGEC, and the results indicated that GGEC strengthened the intestinal barrier by up-regulating protein expression of tight junctions and limiting inflammatory responses.

scholarly journals Anethole Attenuates Enterotoxigenic Escherichia coli-Induced Intestinal Barrier Disruption and Intestinal Inflammation via Modification of TLR Signaling and Intestinal Microbiota

2021 ◽  
Vol 12 ◽  
Author(s):  
Qingyuan Yi ◽  
Jiaxin Liu ◽  
Yufeng Zhang ◽  
Hanzhen Qiao ◽  
Fang Chen ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Growth Performance ◽  
Mrna Expression ◽  
Intestinal Microbiota ◽  
Barrier Function ◽  
Intestinal Inflammation ◽  
Intestinal Barrier ◽  
Intestinal Barrier Function ◽  
Weaned Piglets ◽  
Tnf Α

This study aimed to investigate the effects of dietary anethole supplementation on the growth performance, intestinal barrier function, inflammatory response, and intestinal microbiota of piglets challenged with enterotoxigenic Escherichia coli K88. Thirty-six weaned piglets (24 ± 1 days old) were randomly allocated into four treatment groups: (1) sham challenge (CON); (2) Escherichia coli K88 challenge (ETEC); (3) Escherichia coli K88 challenge + antibiotics (ATB); and (4) Escherichia coli K88 challenge + anethole (AN). On day 12, the piglets in the ETEC, ATB, and AN group were challenged with 10 mL E. coli K88 (5 × 109 CFU/mL), whereas the piglets in the CON group were orally injected with 10 mL nutrient broth. On day 19, all the piglets were euthanized for sample collection. The results showed that the feed conversion ratio (FCR) was increased in the Escherichia coli K88-challenged piglets, which was reversed by the administration of antibiotics or anethole (P < 0.05). The duodenum and jejunum of the piglets in ETEC group exhibited greater villous atrophy and intestinal morphology disruption than those of the piglets in CON, ATB, and AN groups (P < 0.05). Administration of anethole protected intestinal barrier function and upregulated mucosal layer (mRNA expression of mucin-1 in the jejunum) and tight junction proteins (protein abundance of ZO-1 and Claudin-1 in the ileum) of the piglets challenged with Escherichia coli K88 (P < 0.05). In addition, administration of antibiotics or anethole numerically reduced the plasma concentrations of IL-1β and TNF-α (P < 0.1) and decreased the mRNA expression of TLR5, TLR9, MyD88, IL-1β, TNF-α, IL-6, and IL-10 in the jejunum of the piglets after challenge with Escherichia coli K88 (P < 0.05). Dietary anethole supplementation enriched the abundance of beneficial flora in the intestines of the piglets. In summary, anethole can improve the growth performance of weaned piglets infected by ETEC through attenuating intestinal barrier disruption and intestinal inflammation.

scholarly journals PSVIII-1 Nutrient starvation induces autophagy and alters intestinal barrier function in IPEC-J2 cells

2019 ◽  
Vol 97 (Supplement_3) ◽  
pp. 284-284
Author(s):  
Enkai Li ◽  
Hang Lu ◽  
Kolapo Ajuwon
Keyword(s):  
Tight Junction ◽  
Mrna Expression ◽  
Barrier Function ◽  
Intestinal Barrier ◽  
Nutrient Starvation ◽  
Intestinal Barrier Function ◽  
Control Group ◽  
Protein Abundance ◽  
Junction Protein ◽  
Food Antigens

Abstract Autophagy is a cellular process of controlled degradation of damaged organelles and cytoplasmic macromolecules during stress for maintaining homeostasis. Intestinal epithelial cells are barriers against microorganisms, toxins and food antigens. Whether autophagy plays a role in regulating intestinal barrier function is unclear. The objective of this study was to characterize the role of autophagy in starvation-induced alteration of tight junction protein abundance and function in IPEC-J2 cells. Cells were nutrient starved in Krebs-Ringer bicarbonate (KRB) buffer for 0, 0.5, 1, 2, 3, 6, 9 and 12 h. Expression of genes implicated in autophagy regulation (AMPK, MDM2, p53 and DRAM) was determined by RT-PCR. The ratio of protein abundance of microtubule-associated protein light chain 3 (LC3-II/LC3-I) and p62, positive and negative markers of autophagy induction, respectively, was determined by western blotting. Compared with control group (0 h), the relative mRNA expression level of AMPK, MDM2, p53 and DRAM significantly decreased by an average of 52.5% (P < 0.01). Relative to 0 h, the mRNA expression of claudin 1 and claudin 4 significantly increased (108.0%) up to 6 h of starvation and then decreased (31.4%) thereafter (P < 0.01). On the contrary, abundance of claudin 1 and claudin 4 protein was downregulated (49.5%) up to 3 h of starvation and then increased (82.6%) thereafter (P < 0.01). Protein expression of claudin 3 was reduced (P < 0.01) with duration of starvation. There was no change in the protein level of occludin and ZO-1. The ratio of LC3-II/LC3-I significantly increased with duration starvation (P < 0.01), whereas p62 and phospho-AMPK levels decreased up to 6 h of starvation and then increased thereafter (P < 0.01). In summary, autophagy may be implicated in the regulation of tight junction integrity during nutrient starvation in IPEC-J2 cells.

scholarly journals Clostridium Butyricum ZJU-F1 Benefits the Intestinal Barrier Function and Immune Response Associated with Its Modulation of Gut Microbiota in Weaned Piglets

Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 527
Author(s):  
Jie Fu ◽  
Tenghao Wang ◽  
Xiao Xiao ◽  
Yuanzhi Cheng ◽  
Fengqin Wang ◽  
...  
Keyword(s):  
Immune Response ◽  
Bacillus Licheniformis ◽  
Barrier Function ◽  
Intestinal Barrier ◽  
Clostridium Butyricum ◽  
Intestinal Barrier Function ◽  
Weaned Piglets ◽  
Total Acid ◽  
Junction Protein ◽  
Mucin Expression

This study investigated the effects of dietary C. butyricum ZJU-F1 on the apparent digestibility of nutrients, intestinal barrier function, immune response, and microflora of weaned piglets, with the aim of providing a theoretical basis for the application of Clostridium butyricum as an alternative to antibiotics in weaned piglets. A total of 120 weanling piglets were randomly divided into four treatment groups, in which piglets were fed a basal diet supplemented with antibiotics (CON), Bacillus licheniformis (BL), Clostridium butyricum ZJU-F1 (CB), or Clostridium butyricum and Bacillus licheniformis (CB-BL), respectively. The results showed that CB and CB-BL treatment increased the intestinal digestibility of nutrients, decreased intestinal permeability, and increased intestinal tight junction protein and mucin expression, thus maintaining the integrity of the intestinal epithelial barrier. CB and CB-BL, as exogenous probiotics, were also found to stimulate the immune response of weaned piglets and improve the expression of antimicrobial peptides in the ileum. In addition, dietary CB and CB-BL increased the proportion of Lactobacillus. The levels of butyric acid, propionic acid, acetic acid, and total acid were significantly increased in the ceca of piglets fed CB and CB-BL. Furthermore, we validated the effects of C. butyricum ZJU-F1 on the intestinal barrier function and immune response in vitro and found C. butyricum ZJU-F1 improved intestinal function and enhanced the TLR-2-MyD88-NF-κB signaling.

scholarly journals The mRNA-binding protein IGF2BP1 maintains intestinal barrier function by up-regulating occludin expression

2020 ◽  
Vol 295 (25) ◽  
pp. 8602-8612
Author(s):  
Vikash Singh ◽  
Chethana P. Gowda ◽  
Vishal Singh ◽  
Ashwinkumar S. Ganapathy ◽  
Dipti M. Karamchandani ◽  
...  
Keyword(s):  
Intestinal Epithelium ◽  
Barrier Function ◽  
Binding Protein ◽  
Intestinal Barrier ◽  
Intestinal Barrier Function ◽  
Intestinal Epithelial ◽  
Adult Mice ◽  
Junction Protein ◽  
Mrna Binding Protein ◽  
Mrna Binding

Insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1) is an mRNA-binding protein that has an oncofetal pattern of expression. It is also expressed in intestinal tissue, suggesting that it has a possible role in intestinal homeostasis. To investigate this possibility, here we generated Villin CreERT2:Igf2bp1flox/flox mice, which enabled induction of an IGF2BP1 knockout specifically in intestinal epithelial cells (IECs) of adult mice. Using gut barrier and epithelial permeability assays and several biochemical approaches, we found that IGF2BP1 ablation in the adult intestinal epithelium causes mild active colitis and mild-to-moderate active enteritis. Moreover, the IGF2BP1 deletion aggravated dextran sodium sulfate–induced colitis. We also found that IGF2BP1 removal compromises barrier function of the intestinal epithelium, resulting from altered protein expression at tight junctions. Mechanistically, IGF2BP1 interacted with the mRNA of the tight-junction protein occludin (Ocln), stabilizing Ocln mRNA and inducing expression of occludin in IECs. Furthermore, ectopic occludin expression in IGF2BP1-knockdown cells restored barrier function. We conclude that IGF2BP1-dependent regulation of occludin expression is an important mechanism in intestinal barrier function maintenance and in the prevention of colitis.

scholarly journals Lubiprostone Induces Claudin-1 and Protects Intestinal Barrier Function

Pharmacology ◽  
2019 ◽  
Vol 105 (1-2) ◽  
pp. 102-108 ◽  
Author(s):  
Norio Nishii ◽  
Tadayuki Oshima ◽  
Min Li ◽  
Hirotsugu Eda ◽  
Kumiko Nakamura ◽  
...  
Keyword(s):  
Barrier Function ◽  
Intestinal Barrier ◽  
Fluorescein Isothiocyanate ◽  
Intestinal Barrier Function ◽  
Epithelial Barrier ◽  
Dependent Manner ◽  
Epithelial Permeability ◽  
Epithelial Barrier Function ◽  
Dose Dependent

Introduction: Lubiprostone, a chloride channel activator, is said to reduce epithelial permeability. However, whether lubiprostone has a direct effect on the epithelial barrier function and how it modulates the intestinal barrier function remain unknown. Therefore, the effects of lubiprostone on intestinal barrier function were evaluated in vitro. Methods: Caco-2 cells were used to assess the intestinal barrier function. To examine the expression of claudins, immunoblotting was performed with specific antibodies. The effects of lubiprostone on cytokines (IFNγ, IL-6, and IL-1β) and aspirin-induced epithelial barrier disruption were assessed by transepithelial electrical resistance (TEER) and fluorescein isothiocyanate (FITC) labeled-dextran permeability. Results: IFNγ, IL-6, IL-1β, and aspirin significantly decreased TEER and increased epithelial permeability. Lubiprostone significantly improved the IFNγ-induced decrease in TEER in a dose-dependent manner. Lubiprostone significantly reduced the IFNγ-induced increase in FITC labeled-dextran permeability. The changes induced by IL-6, IL-1β, and aspirin were not affected by lubiprostone. The expression of claudin-1, but not claudin-3, claudin-4, occludin, and ZO-1 was significantly increased by lubiprostone. Conclusion: Lubiprostone significantly improved the IFNγ-induced decrease in TEER and increase in FITC labeled-dextran permeability. Lubiprostone increased the expression of claudin-1, and this increase may be related to the effect of lubiprostone on the epithelial barrier function.

scholarly journals Anti-TNF-α antibodies improve intestinal barrier function in Crohn's disease

2012 ◽  
Vol 6 (4) ◽  
pp. 464-469 ◽  
Author(s):  
Rainer Noth ◽  
Eckhard Stüber ◽  
Robert Häsler ◽  
Susanna Nikolaus ◽  
Tanja Kühbacher ◽  
...  
Keyword(s):  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Barrier Function ◽  
Intestinal Barrier ◽  
Intestinal Barrier Function ◽  
Tnf Α

scholarly journals Fenretinide Improves Intestinal Barrier Function and Mitigates Alcohol Liver Disease

2021 ◽  
Vol 12 ◽  
Author(s):  
Xiao-Han Tang ◽  
Marta Melis ◽  
Karen Mai ◽  
Lorraine J. Gudas ◽  
Steven E. Trasino
Keyword(s):  
Liver Disease ◽  
Liver Injury ◽  
Intestinal Permeability ◽  
Kupffer Cells ◽  
Barrier Function ◽  
Intestinal Barrier ◽  
Intestinal Barrier Function ◽  
Protein Levels ◽  
Tnf Α ◽  
Alcohol Liver Disease

Alcohol liver disease (ALD) is a major cause of liver-related mortality globally, yet there remains an unmet demand for approved ALD drugs. The pathogenesis of ALD involves perturbations to the intestinal barrier and subsequent translocation of bacterial endotoxin that, acting through toll-like receptor 4 (TLR4), promotes hepatic inflammation and progression of ALD. In the present study we investigated the ability of fenretinide (Fen) [N-(4-hydroxyphenyl) retinamide], a synthetic retinoid with known anti-cancer and anti-inflammatory properties, to modulate intestinal permeability and clinical hallmarks of ALD in a mouse model of chronic ethanol (EtOH) exposure. Our results show that EtOH-treated mice had reductions in mRNA and protein expression of intestinal tight junction proteins, including claudin one and occludin, and increases in intestinal permeability and endotoxemia compared to pair-fed mice. Also, EtOH-treated mice had marked increases in hepatic steatosis, liver injury, and expression of pro-inflammatory mediators, including TNF-α, and TLR4-positive macrophages, Kupffer cells, and hepatocytes in the intestines and liver, respectively. In contrast, EtOH + Fen-treated mice were resistant to the effects of EtOH on promoting intestinal permeability and had higher intestinal protein levels of claudin one and occludin. Also, EtOH + Fen-treated mice had significantly lower plasma levels of endotoxin, and reductions in expression of TNF-α and TLR4 positive macrophages, Kupffer cells, and hepatocytes in the intestine and liver. Lastly, we found that EtOH + Fen-treated mice exhibited major reductions in hepatic triglycerides, steatosis, and liver injury compared to EtOH-treated mice. Our findings are the first to demonstrate that Fen possesses anti-ALD properties, potentially through modulation of the intestinal barrier function, endotoxemia, and TLR4-mediated inflammation. These data warrant further pre-clinical investigations of Fen as a potential anti-ALD drug.

scholarly journals Gut microbiota regulates AML via alternation of intestinal barrier function mediated by butyrate

2021 ◽  
Author(s):  
Ruiqing Wang ◽  
Xinyu Yang ◽  
Jinting Liu ◽  
Fang Zhong ◽  
Chen Zhang ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Barrier Function ◽  
Fecal Microbiota Transplantation ◽  
Therapeutic Option ◽  
Leukemia Cell ◽  
Intestinal Barrier ◽  
Intestinal Barrier Function ◽  
Significant Shift ◽  
Dependent Manner ◽  
Intestinal Microbes

Abstract The gut microbiota has been linked to many cancers, yet the role of intestinal microbes in acute myeloid leukemia (AML) progression remains unclear. Here, we observed a significant shift in the gut microbiota in AML patients, characterized by reduced Faecalibacterium abundance. According to a murine AML model, we found that intestinal microbial diversity decreased as the disease progressed. On the other side, gut microbiota dysbiosis induced by antibiotic treatment accelerated AML progression with a higher leukemia cell burden and shorter overall survival (OS), while fecal microbiota transplantation altered this process. Metabolome analyses showed that microbiota-derived butyrate concentration obviously decreased in AML patient feces, and butyrate gavage postponed AML progression in a mouse model. Moreover, our study revealed that intestinal barrier function is decreased in AML mice which may be related to the microbiota disorder caused by AML. Lower intestinal barrier function increased the bacterial-associated lipopolysaccharide (LPS) concentration in the peripheral blood of AML patients or mice through enhancing intestinal permeability. Butyrate repaired the intestinal barrier damage and inhibited LPS absorption in AML mice. Collectively, these findings demonstrate that the gut microbiota promotes AML progression in a metabolite dependent manner, and targeting the gut microbiota might provide a novel therapeutic option for AML.

scholarly journals Dietary Fiber Ameliorates Lipopolysaccharide-Induced Intestinal Barrier Function Damage in Piglets by Modulation of Intestinal Microbiome

mSystems ◽  
2021 ◽  
Vol 6 (2) ◽  
Author(s):  
Xiao Sun ◽  
Yalei Cui ◽  
Yingying Su ◽  
Zimin Gao ◽  
Xinying Diao ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Growth Performance ◽  
Proinflammatory Cytokines ◽  
Barrier Function ◽  
Intestinal Microflora ◽  
Intestinal Barrier ◽  
Intestinal Morphology ◽  
Intestinal Barrier Function ◽  
Tnf Α

ABSTRACT Weaning of piglets is accompanied by intestinal inflammation, impaired intestinal barrier function, and intestinal microflora disorder. Regulating intestinal microflora structure can directly or indirectly affect intestinal health and host growth and development. However, whether dietary fiber (DF) affects the inflammatory response and barrier function by affecting the intestinal microflora and its metabolites is unclear. In this study, we investigated the role of intestinal microflora in relieving immune stress and maintaining homeostasis using piglets with lipopolysaccharide (LPS)-induced intestinal injury as a model. DF improved intestinal morphology and barrier function, inhibited the expression of inflammatory signal pathways (Toll-like receptor 2 [TLR2], TLR4, and NF-κB) and proinflammatory cytokines (interleukin 1β [IL-1β], IL-6, and tumor necrosis factor alpha [TNF-α]), and upregulated the expression of barrier-related genes (encoding claudin-1, occludin, and ZO-1). The contents of proinflammatory cytokines (IL-1β, IL-6, and TNF-α) and the activity of diamine oxidase in plasma were decreased. Meanwhile, DF had a strong effect on the composition and function of intestinal microflora at different taxonomic levels, the relative abundances of cellulolytic bacteria and anti-inflammatory bacteria were increased, and the concentrations of propionate, butyrate, and total short-chain fatty acids (SCFAs) in intestinal contents were increased. In addition, the correlation analysis also revealed the potential relationship between metabolites and certain intestinal microflora, as well as the relationship between metabolites and intestinal morphology, intestinal gene expression, and plasma cytokine levels. These results indicate that DF improves intestinal barrier function, in part, by altering intestinal microbiota composition and increasing the synthesis of SCFAs, which subsequently alleviate local and systemic inflammation. IMPORTANCE Adding DF to the diet of LPS-challenged piglets alleviated intestinal and systemic inflammation, improved intestinal barrier function, and ultimately alleviated the growth retardation of piglets. In addition, the addition of DF significantly increased the relative abundance of SCFA-producing bacteria and the production of SCFAs. We believe that the improvement of growth performance of piglets with LPS-induced injury can be attributed to the beneficial effects of DF on intestinal microflora and SCFAs, which reduced the inflammatory response in piglets, improving intestinal barrier function and enhancing body health. These research results provide a theoretical basis and guidance for the use of specific fiber sources in the diet to improve intestinal health and growth performance of piglets and thus alleviate weaning stress. Our data also provide insights for studying the role of DF in regulating gastrointestinal function in human infants.

PSX-A-9 Late-Breaking: Effects of farm noise on ileum intestinal barrier function of pullets

2021 ◽  
Vol 99 (Supplement_3) ◽  
pp. 367-367
Author(s):  
Chun Li ◽  
Runxiang Zhang ◽  
Hanlin Yu ◽  
Yanru Feng ◽  
Jianhong Li ◽  
...  
Keyword(s):  
Barrier Function ◽  
Intestinal Barrier ◽  
Animal Husbandry ◽  
Low Noise ◽  
Intestinal Barrier Function ◽  
Control Group ◽  
Tissue Samples ◽  
Real Time Quantitative Pcr ◽  
Junction Protein ◽  
Related Proteins

Abstract Noise is a potential but not negligible environmental factor in animal husbandry. To investigate the effects of farm noise on intestinal barrier function of pullets, 336 Hailanhe pullets aged 1 day were randomly divided into 3 groups: control group (CON), low noise group (LN), high noise group (HN). LN group and HN group were exposed to noise respectively at 65–75 dB and 85–95 dB, the average and the range of the highest loudness of noise in laying hens’ farms for 6h every day (7:00-19:00, hourly intervals for one hour) and lasted 4 weeks. Non additional noise addition in CON group, noise loudness of which was less than 40dB. 6 birds were randomly chosen form each group after every week of noise stimulation for ileum tissue samples. Hematoxylin-eosin stain (HE stain), immunofluorescence, and real-time quantitative PCR (qRT-PCR) were used to determine changes in ileum structure, expression of intestinal barrier related proteins and mRNAs and HSPs. Results shown that 1 week and 2 weeks after noise exposed inflammatory cell infiltration reduced, the expression of intestinal barrier related proteins (Occludin, Mucin2 and ZO-1) and mRNAs (Claudin-1, Claudin-4, E-cadherin, Occludin, Mucin2, ZO-1 and ZO-2) were significantly increased (P < 0.05), the mRNA expression of HSPs decreased (P < 0.05) or have no significate changes (P > 0.05). After 4 weeks of noise treatment, the expression of mRNAs of intestinal tight junction protein and mucin, HSPs were significantly decreased (P < 0.05). There was no difference between the LN and HN groups on those indicators (P > 0.05). The study indicates that noise at 65-75dB and 85-95dB does not cause stress to ileum of pullets while promote the development of intestinal barrier of chicks within 2 weeks maybe by mild stimulation and birds restored to balance due to habitualization after 4 weeks of noise treatment.

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