scholarly journals Dusp6 Depletion Enhances Gut Barrier Integrity and Microbiota Eubiosis Against Dextran Sulfate Sodium-Induced Colitis in Mice

2020 ◽  
Author(s):  
Cherng-Shyang Chang ◽  
Yi-Chu Liao ◽  
Chih-Ting Huang ◽  
Chiao-Mei Lin ◽  
Chantal Hoi Yin Cheung ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Fecal Microbiota Transplantation ◽  
Fecal Microbiota ◽  
Protective Effects ◽  
Gut Barrier ◽  
Barrier Integrity ◽  
Altered Glucose ◽  
Deficient Mice

Abstract Background: Leaky gut and microbiota dysbiosis have been linked to many chronic inflammatory diseases. Strengthening the gut epithelial barrier is a novel but overlooked strategy for management of gut microbiota-associated illnesses. Results: Using the dextran sulfate sodium (DSS)-induced gut barrier injury-based colitis model, we found that DSS-induced weight loss, rectal bleeding, and colonic epithelium damage were ameliorated in dual-specificity phosphatase 6 (Dusp6)-deficient mice. These protective effects could be attributed to the enhanced colon barrier integrity conferred by Dusp6-deficiency. Consistently, DUSP6 mutation in Caco-2 cells elevated transepithelial electrical resistance, enhanced tight-junctions, and increased expression of microvilli-associated genes. DUSP6-deficient Caco-2 cells also showed increased mitochondrial oxygen consumption accompanied by altered glucose metabolism and decreased glycolysis. Remarkably, our microbiome analysis found that Dusp6-deficient mice harbored fewer pathobionts and facultative anaerobes and more obligate anaerobes than wild-type mice after DSS treatment. Our cohousing and fecal microbiota transplantation experiments demonstrated that the gut/fecal microbiota derived from Dusp6-deficient mice also conferred protection against colitis.Conclusion: We have thus identified Dusp6 deficiency as beneficial in enhancing gut barrier integrity, elevating epithelial phosphoxidation, and maintaining the gut microbiota eubiosis necessary to protect against colitis.

scholarly journals The effect of Sennoside A on the improvement of lipopolysaccharide -associated encephalopathy through gut microbiota

2021 ◽  
Author(s):  
Suyan Li ◽  
Fenyan Zhang ◽  
Yiguang Lin ◽  
Xiaoli Niu ◽  
Jian Lv ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Fecal Microbiota Transplantation ◽  
Intestinal Flora ◽  
Fecal Microbiota ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Microbial Composition ◽  
Germ Free ◽  
Sd Rats ◽  
Tnf Α

Abstract Background Accumulating evidence suggests that the intestinal flora is involved in many neurodegenerative diseases. Sepsis can lead to severe intestinal flora imbalance and brain dysfunction. In this study, we investigated Sennoside A may relieve lipopolysaccharide(LPS)-associated encephalopathy via its effect on the gut microbiota in rats. Methods Adult male Sprague-Dawley (SD) rats and germ free (GF) rats were used. The ordinary and germ free SD rats were adopted as a LPS-associated encephalopathy model with or without Sennoside A administration. We investigated gut microbiota diversity and structure, conducted electroencephalograms (EEG) and measured the levels of TNF-α, IL-1β and IL-6 in the cortexes of Sprague Dawley (SD) rats with or without Sennoside A administration. Horizontal fecal microbiota transplantation (FMT) and germ-free rats were used to confirm the important roles of gut microbiota in the mitigation of LPS-associated encephalopathy in rats after Sennoside A supplementation. Results We found that Sennoside A treatment markedly improved brain function in septic rats including decreased ratios of abnormal EEG and lowered levels of TNF-α, IL-1β, and IL-6 in the rat cortexes. While the gut microbiota changed in septic SD rats, Sennoside A improved gut microbial composition, which might mediate its brain protective effects in sepsis. Sennoside A also reduced inflammation in the cortexes of septic rats via gut microbiota improvement. In germ-free rats that received lipopolysaccharide(LPS),Sennoside A could not lower the ratios of abnormal EEG, and could not alleviate TNF-α, IL-1β, and IL-6 levels in the rats’ cortexes. FMT lowered the ratios of abnormal EEG and alleviate TNF-α, IL-1β, and IL-6 levels in rats’ cortexes, which confirmed our hypothesis that the effect of Sennoside A on the improvement of LPS-associated encephalopathy through gut microbiota. Conclusion Our data confirm our hypothesis that Sennoside A likely exerts its brain protective effects through gut microbiota alteration.

scholarly journals Saccharomyces cerevisiae Fermentation Product Did Not Attenuate Clinical Signs, but Psyllium Husk Has Protective Effects in a Murine Dextran Sulfate Sodium–Induced Colitis Model

2020 ◽  
Vol 4 (11) ◽  
Author(s):  
Ching-Yen Lin ◽  
Anne H Lee ◽  
Karen K Chiu ◽  
Miranda D Vieson ◽  
Andrew J Steelman ◽  
...  
Keyword(s):  
Gene Expression ◽  
Saccharomyces Cerevisiae ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Clinical Signs ◽  
Fecal Microbiota ◽  
Protective Effects ◽  
Psyllium Husk ◽  
Saccharomyces Cerevisiae Fermentation Product ◽  
Colitis Model

ABSTRACT Background Yeast products and psyllium husk may provide relief from clinical signs of colitis due to their ability to promote gut integrity, modulate gut microbiota, or positively affect immune responses, which have been demonstrated in several species. Objective The objective of this study was to investigate the effects of a Saccharomyces cerevisiae fermentation product (SCFP) and psyllium husk (PH) on cecal and fecal microbiota, colonic gene expression and histopathology, and mesenteric lymph node (MLN) immune cells in a dextran sulfate sodium (DSS)–induced colitis model. Methods Male C57BL/6J mice (n = 54) were assigned to a control, 5% SCFP, or 5% PH diet. After 2 wk of diet adaptation, mice were provided distilled water or 3% (wt:vol) DSS for 5 d ad libitum. Body weight, food and water intakes, and disease activity index (DAI) were recorded daily during the treatment period. Fresh fecal samples were collected before and during treatment for microbial analyses. After treatment, mice were killed, followed by tissue collection. Tissues were stored in proper solutions until further analyses. Data were analyzed using the Mixed Models procedure of SAS 9.4 (SAS Institute). Results Consumption of SCFP increased (P < 0.05) species richness of the gut microbiota and relative abundance of Butyricicoccus in fecal and cecal samples compared with control or PH mice. PH mice had greater (P < 0.05) gene expression of claudin (Cldn) 2, Cldn3, Cldn8, and occludin(Ocln) compared with control mice. DAI, MLN immune cell populations, colonic histopathology, and colonic gene expression were not affected (P > 0.05) by SCFP in DSS mice. DSS mice consuming PH had lower (P < 0.05) DAI compared with control or SCFP mice. Conclusions Results suggest that, despite the modest changes it had on cecal and fecal microbiota, SCFP did not attenuate clinical signs associated with DSS-induced colitis in mice, while PH showed protective effects.

The dietary supplement Rhodiola crenulata extract alleviates dextran sulfate sodium-induced colitis in mice through anti-inflammation, mediating gut barrier integrity and reshaping the gut microbiome

2021 ◽  
Vol 12 (7) ◽  
pp. 3142-3158
Author(s):  
Yi Wang ◽  
Hongxun Tao ◽  
Huimin Huang ◽  
Yaqin Xiao ◽  
Xiaoxiao Wu ◽  
...  
Keyword(s):  
Dietary Supplement ◽  
Gut Microbiome ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Gut Barrier ◽  
Barrier Integrity ◽  
Rhodiola Crenulata ◽  
Anti Inflammation

Rhodiola crenulata extract alleviates DSS-induced colitis in mice through anti-inflammation, mediating gut barrier integrity and reshaping the gut microbiome.

scholarly journals Dietary Taxifolin Protects Against Dextran Sulfate Sodium-Induced Colitis via NF-κB Signaling, Enhancing Intestinal Barrier and Modulating Gut Microbiota

2021 ◽  
Vol 11 ◽  
Author(s):  
Jinxiu Hou ◽  
Mingyang Hu ◽  
Le Zhang ◽  
Ya Gao ◽  
Libao Ma ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Immunoglobulin A ◽  
Intestinal Barrier ◽  
Mapk Signaling ◽  
Protective Effects ◽  
Gut Health ◽  
Beneficial Effects ◽  
Rdna Sequencing

Taxifolin is a natural antioxidant polyphenol with various bioactivities and has many beneficial effects on human gut health. However, little is known of its function on colitis. In this study, the protective effects of taxifolin on colitis symptoms, inflammation, signaling pathways, and colon microbiota were investigated using dextran sulfate sodium (DSS)-induced colitis mice. Intriguingly, pre-administration of taxifolin alleviated the colitis symptoms and histological changes of the DSS-challenged mice. Supplementation of taxifolin significantly inhibited the secretions of tumor necrosis factor-α, interleukin (IL)-1β, and IL-6 and significantly increased the secretions of IL-10, secretory immunoglobulin A, superoxide dismutase, and immunoglobulins (IgA, IgG, and IgM) in DSS-induced colitis mice. In addition, the activation of nuclear factor kappa B (NF-κB; p65 and IκBα) signaling was significantly suppressed by taxifolin supplementation. The expression of tight junction proteins (claudin-1 and occludin) was significantly increased by taxifolin. Moreover, 16S rDNA sequencing revealed that the DSS-induced changes of colon microbiota composition and microbial functions (amino acid metabolism and MAPK signaling) were restored by taxifolin, including the decreases of the abundances of Bacteroides, Clostridium ramosum, Clostridium saccharogumia, Sphingobacterium multivorum, and the ratio of Bacteroidetes/Firmicutes, and the increases of the abundances of Desulfovibrio C21 c20 and Gemmiger formicilis at species level. In conclusion, these results revealed that dietary taxifolin has a great potential to prevent colitis by inhibiting the NF-κB signaling pathway, enhancing intestinal barrier, and modulating gut microbiota.

scholarly journals Anti-Inflammatory Effects of Heritiera littoralis Fruits on Dextran Sulfate Sodium- (DSS-) Induced Ulcerative Colitis in Mice by Regulating Gut Microbiota and Suppressing NF-κB Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-20
Author(s):  
Guosheng Lin ◽  
Minyao Li ◽  
Nan Xu ◽  
Xiaoli Wu ◽  
Jingjing Liu ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Gut Microbiota ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Activity Index ◽  
Disease Activity Index ◽  
Rrna Gene ◽  
Chemical Compositions ◽  
Protective Effects ◽  
Esi Ms

Aim of the Study. This study is aimed at exploring the effects and pharmacological mechanisms of the extracts from the Heritiera littoralis fruit (EFH) on dextran sulfate sodium- (DSS-) induced ulcerative colitis (UC) in mice. Materials and Methods. The chemical compositions of EFH were identified using LC-ESI-MS. The mice with 3% DSS-induced UC were administered EFH (200, 400, and 800 mg/kg), sulfasalazine (SASP, 200 mg/kg), and azathioprine (AZA, 13 mg/kg) for 10 days via daily gavage. The colonic inflammation was evaluated by the disease activity index (DAI), colonic length, histological scores, and levels of inflammatory mediators. The gut microbiota was characterized by 16S rRNA gene sequencing and analysis. Results. LC-ESI-MS analysis showed that EFH was rich in alkaloids and flavones. The results indicated that EFH significantly improved the DAI score, relieved colon shortening, and repaired pathological colonic variations in colitis. In addition, proteins in the NF-κB pathway were significantly inhibited by EFH. Furthermore, EFH recovered the diversity and balance of the gut microbiota. Conclusions. EFH has protective effects against DSS-induced colitis by keeping the balance of the gut microbiota and suppressing the NF-κB pathway.

scholarly journals Fecal Microbiota Transplantation Beneficially Regulates Intestinal Mucosal Autophagy and Alleviates Gut Barrier Injury

mSystems ◽  
2018 ◽  
Vol 3 (5) ◽  
Author(s):  
Saisai Cheng ◽  
Xin Ma ◽  
Shijie Geng ◽  
Xuemei Jiang ◽  
Yuan Li ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Acid Metabolism ◽  
Fecal Microbiota Transplantation ◽  
Fecal Microbiota ◽  
Intestinal Morphology ◽  
Rrna Gene ◽  
Microbial Structure ◽  
Gut Barrier ◽  
Content Type ◽  
E Coli

ABSTRACT Fecal microbiota transplantation (FMT) is one of the most effective ways to regulate the gut microbiota. Here, we investigated the effect of exogenous fecal microbiota on gut function from the perspective of analysis of the mucosal proteomes in a piglet model. A total of 289 differentially expressed proteins were annotated with 4,068 gene ontology (GO) function entries in the intestinal mucosa, and the levels of autophagy-related proteins in the forkhead box O (FoxO) signaling pathway were increased whereas the levels of proteins related to inflammation response were decreased in the recipient. Then, to assess the alleviation of epithelial injury in the Escherichia coli K88-infected piglets following FMT, intestinal microbiome-metabolome responses were determined. 16S rRNA gene sequencing showed that the abundances of beneficial bacteria, such as Lactobacillus and Succinivibrio, were increased whereas those of Enterobacteriaceae and Proteobacteria bacteria were decreased in the infected piglets following FMT. Metabolomic analysis revealed that levels of 58 metabolites, such as lactic acid and succinic acid, were enhanced in the intestinal lumen and that seven metabolic pathways, such as branched-chain amino acid metabolism pathways, were upregulated in the infected piglets following FMT. In concordance with the metabolome data, results of metagenomics prediction analysis also demonstrated that FMT modulated the metabolic functions of gut microbiota associated with linoleic acid metabolism. In addition, intestinal morphology was improved, a result that coincided with the decrease of intestinal permeability and the enhancement of mucins and mucosal expression of tight junction proteins in the recipient. Taken together, the results showed that FMT triggered intestinal mucosal protective autophagy and alleviated gut barrier injury through alteration of the gut microbial structure. IMPORTANCE The gut microbiota plays a crucial role in human and animal health, and its disorder causes multiple diseases. Over the past decade, FMT has gained increasing attention due to the success in treating Clostridium difficile infection (CDI) and inflammatory bowel disease (IBD). Although FMT appears to be effective, how FMT functions in the recipient remains unknown. Whether FMT exerts this beneficial effect through a series of changes in the host organism caused by alteration of gut microbial structure is also not known. In the present study, newborn piglets and E. coli K88-infected piglets were selected as models to explore the interplay between host and gut microbiota following FMT. Our results showed that FMT triggered intestinal mucosal autophagy and alleviated gut barrier injury caused by E. coli K88. This report provides a theoretical basis for the use of FMT as a viable therapeutic method for gut microbial regulation.

scholarly journals β-Sitosterol Ameliorates Endometrium Receptivity in PCOS-Like Mice: The Mediation of Gut Microbiota

2021 ◽  
Vol 8 ◽  
Author(s):  
Yanyan Yu ◽  
Ying Cao ◽  
Wenling Huang ◽  
Yanxia Liu ◽  
Ying Lu ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Fecal Microbiota Transplantation ◽  
Polycystic Ovary ◽  
Fecal Microbiota ◽  
Pathological Process ◽  
Endometrial Receptivity ◽  
Enzyme Linked Immunosorbent Assay ◽  
Protective Effects ◽  
Childbearing Age ◽  
Cox 2

Background: Polycystic ovary syndrome (PCOS), one of the most common endocrine diseases in women of childbearing age, has been found to be accompanied by changes in the gut microbiota. The Bu Shen Yang Xue formula (BSYXF) is a traditional Chinese medicine widely used for the treatment of PCOS. This study aimed to investigate whether the protective effects of β-sitosterol, the main active ingredient of BSYXF, on PCOS was mediated by regulating gut microbiota.Methods: The presence of β-sitosterol in BSYXF was detected by liquid chromatography-mass spectrometry. The PCOS-like mouse model was induced by dehydroepiandrosterone. The fecal supernatant of β-sitosterol-treated mice was prepared for fecal microbiota transplantation (FMT). Body weight and wet weight of the uterus and ovary of the mice were recorded for organ index calculation. Hematoxylin and eosin stain was used to assess the endometrial morphology and microenvironment changes. Expression of endometrial receptivity markers cyclooxygenase-2 (COX-2), Integrin ανβ3, leukemia inhibitory factor (LIF), and homeobox A10 (HOXA10) in the endometrium were determined by immunohistochemistry and western blot analysis. Enzyme-linked immunosorbent assay was employed to detect the expression of follicle stimulating hormone (FSH), luteinizing hormone (LH), progesterone (P), and testosterone (T) in the serum. The diversity of gut microbiota was examined by 16S rDNA gene sequencing.Results: With the treatment of β-sitosterol and β-sitosterol-FMT, the uterine index of PCOS-like mice increased, the ovarian index decreased, levels of COX-2, LH and T decreased, and levels of Integrin ανβ3, LIF, HOXA10, FSH, and P increased. Under β-sitosterol treatment, the structure of the gut microbiota in PCOS-like mice was also changed.Conclusion: β-sitosterol regulates the endometrial receptivity of PCOS and harmonizes the sex hormone balance, which may be related to the changes in the structure and composition of gut microbiota, thus affecting the pathological process of PCOS.

scholarly journals Oridonin Alters Hepatic Urea Cycle via Gut Microbiota and Protects against Acetaminophen-Induced Liver Injury

2021 ◽  
Vol 2021 ◽  
pp. 1-15
Author(s):  
Mu-keng Hong ◽  
Hai-hua Liu ◽  
Gui-hong Chen ◽  
Jun-qing Zhu ◽  
Song-yuan Zheng ◽  
...  
Keyword(s):  
Liver Injury ◽  
Gut Microbiota ◽  
Urea Cycle ◽  
Fecal Microbiota Transplantation ◽  
Redox Homeostasis ◽  
Fecal Microbiota ◽  
Hepatic Tissue ◽  
Western World ◽  
Related Factor ◽  
Protective Effects

Acetaminophen (APAP) hepatotoxicity is the leading cause of acute liver failure in the western world. Oridonin (OD), which is the major active ingredient of the traditional Chinese medicine Rabdosia rubescens, reportedly exerts anti-inflammatory and antioxidative effects. Here, we first find that OD protects against APAP-induced hepatotoxicity. The results of hepatic tissue-associated RNA-seq and metabolomics showed that the protective effects of OD were dependent upon urea cycle regulation. And such regulation of OD is gut microbiota partly dependent, as demonstrated by fecal microbiota transplantation (FMT). Furthermore, using 16S rRNA sequencing, we determined that OD significantly enriched intestinal Bacteroides vulgatus, which activated the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway to regulate redox homeostasis against APAP by urea cycle. In conclusion, our study suggests that the Bacteroides vulgatus-urea cycle-Nrf2 axis may be a potential target for reducing APAP-induced liver injury, which is altered by OD.

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