scholarly journals Lactulose Improves Neurological Outcomes by Repressing Harmful Bacteria and Regulating Inflammatory Reactions in Mice After Stroke

2021 ◽  
Vol 11 ◽  
Author(s):  
Quan Yuan ◽  
Ling Xin ◽  
Song Han ◽  
Yue Su ◽  
Ruixia Wu ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Metabolic Disorder ◽  
Intestinal Barrier ◽  
Neurological Function ◽  
Inflammatory Factors ◽  
Plasma Metabolites ◽  
Inflammatory Reactions ◽  
Rdna Sequencing ◽  
Photothrombotic Stroke ◽  
Gut Microbiota Dysbiosis

Background and ObjectiveGut microbiota dysbiosis following stroke affects the recovery of neurological function. Administration of prebiotics to counteract post-stroke dysbiosis may be a potential therapeutic strategy to improve neurological function. We aim to observe the effect of lactulose on neurological function outcomes, gut microbiota composition, and plasma metabolites in mice after stroke.MethodsMale C57BL/6 mice (20–25 g) were randomly divided into three groups: healthy control, photothrombotic stroke + triple-distilled water, and photothrombotic stroke + lactulose. After 14 consecutive days of lactulose administration, feces, plasma, and organs were collected. 16S rDNA sequencing, plasma untargeted metabolomics, qPCR, flow cytometry and Elisa were performed.ResultsLactulose supplementation significantly improved the functional outcome of stroke, downregulated inflammatory reaction, and increased anti-inflammatory factors in both the brain and gut. In addition, lactulose supplementation repaired intestinal barrier injury, improved gut microbiota dysbiosis, and partially amended metabolic disorder after stroke.ConclusionLactulose promotes functional outcomes after stroke in mice, which may be attributable to repressing harmful bacteria, and metabolic disorder, repairing gut barrier disruption, and reducing inflammatory reactions after stroke.

scholarly journals Phenazines Modulate Gastrointestinal Metabolism and Microbiota

2021 ◽  
Author(s):  
Wenjing Peng ◽  
Hui Li ◽  
Xiaole Zhao ◽  
Bing Shao ◽  
Kui Zhu
Keyword(s):  
Gut Microbiota ◽  
Digestive Tract ◽  
Metabolic Disorder ◽  
Rational Design ◽  
Pathogenic Bacteria ◽  
Intestinal Barrier ◽  
Swine Model ◽  
Structural Skeleton ◽  
Gut Microbiota Dysbiosis

Abstract Background: Natural and synthetic phenazines are ubiquitously occurred in environment and have been used for various therapeutic purposes in human, animals and agriculture, and the widespread use makes residue problem in environment and foods increasingly serious. However, the metabolic and comprehensive impacts of phenazines on the digestive tract are poorly understood, particularly the microbial pyocyanin (PYO), the most representative phenazines produced by Pseudomonas . Here, we utilized PYO as the representative of phenazines to study the effects on digestive tract. Results: Metabolic kinetic analysis showed that PYO exhibited low oral bioavailability in both rats and swine model, revealing a restriction of PYO in gut and might cause impacts on digestive tract. PYO was subsequently found to induce intestinal barrier destruction including inflammation and reactive oxygen species (ROS) accumulation in duodenum. Microbiome analysis showed that PYO caused gut microbiota dysbiosis by decreasing the symbiotic bacteria and increasing the opportunistic pathogenic bacteria. Additionally, the integral and dysfunctional assessment of liver demonstrated that PYO induced liver inflammation and metabolic disorder. Metabolism analysis further confirmed that PYO could be metabolized by both gut microbiota and liver, and all metabolites retained the nitrogen-containing tricyclic structural skeleton of phenazines, which was the core bioactivity of phenazine compounds, indicating all the outcomes were due to the intrinsic characteristic of phenazine structure. Conclusions: PYO were low oral bioavailable and all the metabolites retained the nitrogen-containing tricyclic structural skeleton, final resulting in the damages to digestive tract including intestinal barrier destruction, gut microbiota dysbiosis, liver damages and metabolic disorder. These findings elucidated the effect of phenazines on digestive tract in vivo and shed light on the rational design of phenazines for the development and application of such compounds in future.

scholarly journals Constipation induced gut microbiota dysbiosis exacerbates experimental autoimmune encephalomyelitis in C57BL/6 mice

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Xiuli Lin ◽  
Yingying Liu ◽  
Lili Ma ◽  
Xiaomeng Ma ◽  
Liping Shen ◽  
...  
Keyword(s):  
Experimental Autoimmune Encephalomyelitis ◽  
Gut Microbiota ◽  
Blood Brain Barrier ◽  
Intestinal Barrier ◽  
Brain Barrier ◽  
Autoimmune Encephalomyelitis ◽  
Gm Csf ◽  
Blood Brain ◽  
Gut Microbiota Dysbiosis ◽  
Experimental Autoimmune

Abstract Background Constipation is a common gastrointestinal dysfunction which has a potential impact on people's immune state and their quality of life. Here we investigated the effects of constipation on experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). Methods Constipation was induced by loperamide in female C57BL/6 mice. The alternations of gut microbiota, permeability of intestinal barrier and blood–brain barrier, and histopathology of colon were assessed after constipation induction. EAE was induced in the constipation mice. Fecal microbiota transplantation (FMT) was performed from constipation mice into microbiota-depleted mice. Clinical scores, histopathology of inflammation and demyelination, Treg/Th17 and Treg17/Teff17 imbalance both in the peripheral lymphatic organs and central nervous system, cytokines include TGF-β, GM-CSF, IL-10, IL-17A, IL-17F, IL-21, IL-22, and IL-23 in serum were assessed in different groups. Results Compared with the vehicle group, the constipation mice showed gut microbiota dysbiosis, colon inflammation and injury, and increased permeability of intestinal barrier and blood–brain barrier. We found that the clinical and pathological scores of the constipation EAE mice were severer than that of the EAE mice. Compared with the EAE mice, the constipation EAE mice showed reduced percentage of Treg and Treg17 cells, increased percentage of Th17 and Teff17 cells, and decreased ratio of Treg/Th17 and Treg17/Teff17 in the spleen, inguinal lymph nodes, brain, and spinal cord. Moreover, the serum levels of TGF-β, IL-10, and IL-21 were decreased while the GM-CSF, IL-17A, IL-17F, IL-22, and IL-23 were increased in the constipation EAE mice. In addition, these pathological processes could be transferred via their gut microbiota. Conclusions Our results verified that constipation induced gut microbiota dysbiosis exacerbated EAE via aggravating Treg/Th17 and Treg17/Teff17 imbalance and cytokines disturbance in C57BL/6 mice.

Benzene exposure induces gut microbiota dysbiosis and metabolic disorder in mice

2020 ◽  
Vol 705 ◽  
pp. 135879 ◽  
Author(s):  
Rongli Sun ◽  
Kai Xu ◽  
Shuangbin Ji ◽  
Yunqiu Pu ◽  
Zhaodi Man ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Metabolic Disorder ◽  
Benzene Exposure ◽  
Gut Microbiota Dysbiosis

scholarly journals The Correlation between Gut Microbiota and Serum Metabolomic in Elderly Patients with Chronic Heart Failure

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Zhenhua Wang ◽  
Zhaoling Cai ◽  
Markus W. Ferrari ◽  
Yilong Liu ◽  
Chengyi Li ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Gut Microbiota ◽  
Elderly Patients ◽  
16S Rdna ◽  
Healthy Subjects ◽  
The Elderly ◽  
Inflammatory Factors ◽  
16S Rdna Sequencing ◽  
Rdna Sequencing

Objective. Chronic heart failure (CHF) refers to a state of persistent heart failure that can be stable, deteriorated, or decompensated. The mechanism and pathogenesis of myocardial remodeling remain unknown. Based on 16S rDNA sequencing and metabolomics technology, this study analyzed the gut microbiota and serum metabolome in elderly patients with CHF to provide new insights into the microbiota and metabolic phenotypes of CHF. Methods. Blood and fecal samples were collected from 25 elderly patients with CHF and 25 healthy subjects. The expression of inflammatory factors in blood was detected by ELISA. 16S rDNA sequencing was used to analyze the changes in microorganisms in the samples. The changes of small molecular metabolites in serum samples were analyzed by LC-MS/MS. Spearman correlation coefficients were used to analyze the correlation between gut microbiota and serum metabolites. Results. Our results showed that the IL-6, IL-8, and TNF-α levels were significantly increased, and the IL-10 level was significantly decreased in the elderly patients with CHF compared with the healthy subjects. The diversity of the gut microbiota was decreased in the elderly patients with CHF. Moreover, Escherichia Shigella was negatively correlated with biocytin and RIBOFLAVIN. Haemophilus was negatively correlated with alpha-lactose, cellobiose, isomaltose, lactose, melibiose, sucrose, trehalose, and turanose. Klebsiella was positively correlated with bilirubin and ethylsalicylate. Klebsiella was negatively correlated with citramalate, hexanoylcarnitine, inosine, isovalerylcarnitine, methylmalonate, and riboflavin. Conclusion. The gut microbiota is simplified by the disease, and serum small-molecule metabolites evidently change in elderly patients with CHF. Serum and fecal biomarkers could be used for elderly patients with CHF screening.

scholarly journals Glucosamine Ameliorates Symptoms of High-Fat Diet-Fed Mice by Reversing Imbalanced Gut Microbiota

2021 ◽  
Vol 12 ◽  
Author(s):  
Xubing Yuan ◽  
Junping Zheng ◽  
Lishi Ren ◽  
Siming Jiao ◽  
Cui Feng ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
High Fat Diet ◽  
Inflammatory Responses ◽  
Fasting Blood Glucose ◽  
Intestinal Barrier ◽  
Intestinal Bacteria ◽  
High Fat ◽  
Lipid Metabolism Disorder ◽  
Metabolism Disorder ◽  
Rdna Sequencing

Glucosamine (GlcN) is used as a supplement for arthritis and joint pain and has been proved to have effects on inflammation, cancer, and cardiovascular diseases. However, there are limited studies on the regulatory mechanism of GlcN against glucose and lipid metabolism disorder. In this study, we treated high-fat diet (HFD)-induced diabetic mice with GlcN (1 mg/ml, in drinking water) for five months. The results show that GlcN significantly reduced the fasting blood glucose of HFD-fed mice and improved glucose tolerance. The feces of intestinal contents in mice were analyzed using 16s rDNA sequencing. It was indicated that GlcN reversed the imbalanced gut microbiota in HFD-fed mice. Based on the PICRUSt assay, the signaling pathways of glucolipid metabolism and biosynthesis were changed in mice with HFD feeding. By quantitative real-time PCR (qPCR) and hematoxylin and eosin (H&E) staining, it was demonstrated that GlcN not only inhibited the inflammatory responses of colon and white adipose tissues, but also improved the intestinal barrier damage of HFD-fed mice. Finally, the correlation analysis suggests the most significantly changed intestinal bacteria were positively or negatively related to the occurrence of inflammation in the colon and fat tissues of HFD-fed mice. In summary, our studies provide a theoretical basis for the potential application of GlcN to glucolipid metabolism disorder through the regulation of gut microbiota.

scholarly journals The Herbal Medicine Scutellaria-Coptis Alleviates Intestinal Mucosal Barrier Damage in Diabetic Rats by Inhibiting Inflammation and Modulating the Gut Microbiota

2020 ◽  
Vol 2020 ◽  
pp. 1-17
Author(s):  
Boxun Zhang ◽  
Rensong Yue ◽  
Yuan Chen ◽  
Xiaoying Huang ◽  
Maoyi Yang ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Intestinal Inflammation ◽  
Intestinal Barrier ◽  
Diabetic Rats ◽  
Mucosal Barrier ◽  
Inflammatory Factors ◽  
Pathological State ◽  
Intestinal Mucosal Barrier ◽  
Metabolic Inflammation ◽  
Anti Inflammatory

Recent studies have confirmed that increased intestinal permeability and gut-origin lipopolysaccharide (LPS) translocation are important causes of metabolic inflammation in type 2 diabetes (T2D), but there are no recognized therapies for targeting this pathological state. Scutellaria baicalensis and Coptis chinensis are a classic herbal pair often used to treat diabetes and various intestinal diseases, and repair of intestinal barrier damage may be at the core of their therapeutic mechanism. This study investigated the effects of oral administration of Scutellaria-Coptis (SC) on the intestinal mucosal barrier in diabetic rats and explored the underlying mechanism from the perspective of anti-inflammatory and gut microbiota-modulatory effects. The main results showed that, in addition to regulating glycolipid metabolism disorders and inhibiting serum inflammatory factors, SC could also upregulate the expression levels of the tight junction proteins claudin-1, occludin, and zonula occludens (ZO-1), significantly improve intestinal epithelial damage, and inhibit excessive LPS translocation into the blood circulation. Furthermore, it was found that SC could reduce the levels of the inflammatory factors interleukin-1β (IL-1β), IL-6, and tumour necrosis factor-α (TNF-α) in intestinal tissue and that the anti-inflammatory effects involved the TLR-4/TRIF and TNFR-1/NF-κB signalling pathways. Moreover, SC had a strong inhibitory effect on some potential enteropathogenic bacteria and LPS-producing bacteria, such as Proteobacteria, Enterobacteriaceae, Enterobacter, Escherichia-Shigella, and Enterococcus, and could also promote the proliferation of butyrate-producing bacteria, such as Lachnospiraceae and Prevotellaceae. Taken together, the hypoglycaemic effects of SC were related to the protection of the intestinal mucosal barrier, and the mechanisms might be related to the inhibition of intestinal inflammation and the regulation of the gut microbiota.

Gut microbiota dysbiosis promotes age-related atrial fibrillation by lipopolysaccharide and glucose-induced activation of NLRP3-inflammasome

2021 ◽  
Author(s):  
Yun Zhang ◽  
Song Zhang ◽  
Bolin Li ◽  
Yingchun Luo ◽  
Yongtai Gong ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Gut Microbiota ◽  
Nlrp3 Inflammasome ◽  
Intestinal Barrier ◽  
Receptor Protein ◽  
Aged Rats ◽  
Atrial Fibrosis ◽  
Glucose Levels ◽  
Age Related ◽  
Gut Microbiota Dysbiosis

Abstract Aims Ageing is the most significant contributor to the increasing prevalence of atrial fibrillation (AF). The gut microbiota dysbiosis is involved in age-related diseases. However, whether the aged-associated dysbiosis contributes to age-related AF is still unknown. Direct demonstration that the aged gut microbiota is sufficient to transmit the enhanced AF susceptibility in a young host via microbiota-intestinal barrier-atria axis has not yet been reported. This study aimed to determine whether gut microbiota dysbiosis affects age-related AF. Methods and results Herein, by using a faecal microbiota transplantation (FMT) rat model, we demonstrated that the high AF susceptibility of aged rats could be transmitted to a young host. Specially, we found the dramatically increased levels of circulating lipopolysaccharide (LPS) and glucose led to the up-regulated expression of NOD-like receptor protein (NLRP)-3 inflammasome, promoting the development of AF, which depended on the enhanced atrial fibrosis in recipient host. Inhibition of inflammasome by a potent and selective inhibitor of the NLRP3 inflammasome, MCC950, resulted in a lower atrial fibrosis and AF susceptibility. Then, we conducted cross-sectional clinical studies to explore the effect of ageing on the altering trends with glucose levels and circulating LPS among clinical individuals in two China hospitals. We found that both of serum LPS and glucose levels were progressively increased in elderly patients as compared with those young. Furthermore, the ageing phenotype of circulating LPS and glucose levels, intestinal structure and atrial NLRP3-inflammasome of rats were also confirmed in clinical AF patients. Finally, aged rats colonized with youthful microbiota restored intestinal structure and atrial NLRP3-inflammasome activity, which suppressed the development of aged-related AF. Conclusions Collectively, these studies described a novel causal role of aberrant gut microbiota in the pathogenesis of age-related AF, which indicates that the microbiota-intestinal barrier-atrial NLRP3 inflammasome axis may be a rational molecular target for the treatment of aged-related arrhythmia disease.

scholarly journals Pathobiological Relationship of Excessive Dietary Intake of Choline/L-Carnitine: A TMAO Precursor-Associated Aggravation in Heart Failure in Sarcopenic Patients

Nutrients ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 3453
Author(s):  
May Nasser Bin-Jumah ◽  
Sadaf Jamal Gilani ◽  
Salman Hosawi ◽  
Fahad A. Al-Abbasi ◽  
Mustafa Zeyadi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Gut Microbiota ◽  
Older Patients ◽  
Blood Circulation ◽  
Intestinal Barrier ◽  
Minimum Level ◽  
Bacterial Strains ◽  
Inflammatory Reactions ◽  
Patients With Heart Failure ◽  
Relationship Of

The microecological environment of the gastrointestinal tract is altered if there is an imbalance between the gut microbiota phylases, resulting in a variety of diseases. Moreover, progressive age not only slows down physical activity but also reduces the fat metabolism pathway, which may lead to a reduction in the variety of bacterial strains and bacteroidetes’ abundance, promoting firmicutes and proteobacteria growth. As a result, dysbiosis reduces physiological adaptability, boosts inflammatory markers, generates ROS, and induces the destruction of free radical macromolecules, leading to sarcopenia in older patients. Research conducted at various levels indicates that the microbiota of the gut is involved in pathogenesis and can be considered as the causative agent of several cardiovascular diseases. Local and systematic inflammatory reactions are caused in patients with heart failure, as ischemia and edema are caused by splanchnic hypoperfusion and enable both bacterial metabolites and bacteria translocation to enter from an intestinal barrier, which is already weakened, to the blood circulation. Multiple diseases, such as HF, include healthy microbe-derived metabolites. These key findings demonstrate that the gut microbiota modulates the host’s metabolism, either specifically or indirectly, by generating multiple metabolites. Currently, the real procedures that are an analogy to the symptoms in cardiac pathologies, such as cardiac mass dysfunctions and modifications, are investigated at a minimum level in older patients. Thus, the purpose of this review is to summarize the existing knowledge about a particular diet, including trimethylamine, which usually seems to be effective for the improvement of cardiac and skeletal muscle, such as choline and L-carnitine, which may aggravate the HF process in sarcopenic patients.

scholarly journals Rhubarb alleviates acute lung injury by modulating gut microbiota dysbiosis in mice

2020 ◽  
Author(s):  
Tingyu Tang ◽  
Fei Wang ◽  
Juan Liu ◽  
Tian Zhao ◽  
Wu Ye ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Gut Microbiota ◽  
Treg Cell ◽  
Lung Tissue ◽  
Pulmonary Inflammation ◽  
Chinese Herb ◽  
Treg Cells ◽  
Rdna Sequencing ◽  
Gut Microbiota Dysbiosis

Abstract Purposes: Intestinal microbiota disorders can aggravate pulmonary inflammation during acute lung injury (ALI). Rhubarb, a Chinese herb, can regulated the gut microbiota. Therefore, this study was conducted to test the hypothesis that rhubarb alleviates gut microbiota dysbiosis and inflammation. Methods: Feces were collected from patients with ALI to detect the gut microbiota using 16S rDNA sequencing. Subsequently, a mouse model of ALI was established using lipopolysaccharide to investigate changes in the gut microbiota, the periperal blood was attained for detecting the Th17/Treg cell ratio, and the effect of rhubarb treatment on the gut microbiota and Th17/Treg ratio were also evaluated. Results: Rhubarb treatment significantly reduced the Firmicutes abundance and markedly increased the Bacteroidetes abundance in ALI patients. The rat models also showed a similar imbalance in the Firmicutes/Bacteroidetes ratio. Rhubarb treatment alleviated the damaged lung tissue, accelerated Firmicutes proliferation, increased the HDAC6 in both the mice lung tissue and serum, and markedly reduced the Treg cells and increased the Th17 cells in the spleen tissue. Conclusion: We determined that both patients with ALI and mouse models of ALI presented gut microbiota dysbiosis and Th17/Treg cell imbalances. Rhubarb promoted Firmicutes proliferation, increased the HDAC6 concentration, restored the Th17/Treg cell balance, and protected against ALI.

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