Gut Microbiota Dysbiosis In Mice Research Articles

Ethanol Extract of Limonium bicolor Improves Dextran Sulfate Sodium-Induced Ulcerative Colitis by Alleviating Inflammation and Restoring Gut Microbiota Dysbiosis in Mice.

Ulcerative colitis (UC) is a kind of inflammatory bowel condition characterized by inflammation within the mucous membrane, rectal bleeding, diarrhea, and pain experienced in the abdominal region. Existing medications for UC have limited treatment efficacy and primarily focus on symptom relief. Limonium bicolor (LB), an aquatic traditional Chinese medicine (TCM), exerts multi-targeted therapeutic effects with few side effects and is used to treat anemia and hemostasis. Nevertheless, the impact of LB on UC and its mechanism of action remain unclear. Therefore, the objective of this study was to investigate the anti-inflammatory effects and mechanism of action of ethanol extract of LB (LBE) in lipopolysaccharide-induced RAW 264.7 macrophages and dextran sulfate sodium (DSS)-induced UC. The results showed that LBE suppressed the secretion of cytokines in LPS-stimulated RAW 264.7 cells in a dose-dependent manner. LBE had protective effects against DSS-induced colitis in mice, decreased the disease activity index (DAI) score, alleviated symptoms, increased colon length, and improved histological characteristics, thus having protective effects against DSS-induced colitis in mice. In addition, it reversed disturbances in the abundance of proteobacteria and probiotics such as Lactobacillus and Blautia in mice with DSS-induced UC. Based on the results of network pharmacology analysis, we identified four main compounds in LBE that are associated with five inflammatory genes (Ptgs2, Plg, Ppar-γ, F2, and Gpr35). These results improve comprehension of the biological activity and functionality of LB and may facilitate the development of LB-based compounds for the treatment of UC.

Fucoxanthin Alleviates Dextran Sulfate Sodium-Induced Colitis and Gut Microbiota Dysbiosis in Mice.

The purpose of this study was to evaluate the preventive role and underlying mechanisms of fucoxanthin (Fx) on dextran sulfate sodium (DSS)-induced colitis in mice. The present data demonstrated that oral administration of Fx (50 and 200 mg/kg body weight/day) for 36 days significantly alleviated the severity of colitis in DSS-treated mice, as evidenced by attenuating body weight loss, bloody stool, diarrhea, shortened colon length, colonic epithelium distortion, a thin mucus layer, goblet cell depletion, damaged crypts, and extensive infiltration of inflammatory cells in the colonic mucosa. Additionally, Fx notably relieved DSS-induced intestinal epithelial barrier dysfunction via maintaining the tight junction function and preventing excessive apoptosis of colonic epithelial cells. Moreover, Fx effectively diminished colonic inflammation and oxidative stress in DSS-treated mice, and its mechanisms might be due to blunting the activation of NF-κB and NLRP3 inflammasome signaling pathways. Furthermore, Fx also modulates DSS-induced gut microbiota dysbiosis via recovering the richness and diversity of gut microbiota and reshaping the structure of gut microbiota, such as increasing the Firmicutes and Bacteroidota (F/B) ratio and elevating the relative abundance of some potential beneficial bacteria, including Lactobacillaceae and Lachnospiraceae. Overall, Fx might be developed as a promising functional ingredient to prevent colitis and maintain intestinal homeostasis.

Glucocorticoid-induced osteoporosis is prevented by dietary prune in female mice.

Glucocorticoid-induced osteoporosis (GIO) is a significant side effect of prolonged glucocorticoid (GC) treatment. Chronic GC treatment also leads to trabecular bone loss and gut microbiota dysbiosis in mice. The gut dysbiosis is mechanistically linked to GIO, which indicates that the microbiota can be targeted to prevent GIO. Prunes, a dried fruit and prebiotic, have emerged in the literature as an effective treatment for sex-steroid deficiency induced osteoporosis (primary osteoporosis). Prunes also significantly alter the composition of the gut microbiota in both rodent models and human studies. Therefore, we tested if dietary prune (DP) supplementation could prevent GC-induced bone loss and affect microbiota composition in an established model of GIO. Sixteen-week-old, skeletally mature, female C57BL/6J mice were treated with a subcutaneous 5mg placebo or prednisolone pellet for 8weeks and fed an AIN-93M control diet or a diet modified to include 5, 15, or 25% (w/w) dried California prune powder. As expected, GC treated mice developed significant trabecular bone loss in the distal femur. More importantly, as little as 5% DP supplementation effectively prevented trabecular bone loss. Further, dose dependent increases in trabecular bone volume fraction were observed in GC + 15% and GC + 25% DP mice. Amazingly, in the placebo (non-GC treated) groups, 25% DP supplementation caused a ∼3-fold increase in distal femur trabecular bone volume fraction; this sizable bone response has not been previously observed in healthy mice with gut targeted natural treatments. Along with the striking effect on bone health, GC treatment and 25% DP supplementation led to drastic shifts in gut microbiota composition and several specific changes are strongly associated with bone health. Taken together, these results are the first to demonstrate that DP supplementation effectively prevents the negative effects of prolonged GC therapy on trabecular bone health and strongly associates with shifts in the composition of the gut microbiota.

The gut microbiota contributes to the infection of bovine viral diarrhea virus in mice.

Bovine viral diarrhea virus (BVDV) is prevalent worldwide and causes significant economic losses. Gut microbiota is a large microbial community and has a variety of biological functions. However, whether there is a correlation between gut microbiota and BVDV infection and what kind of relation between them have not been reported. Here, we found that gut microbiota composition changed in normal mice after infecting with BVDV, but mainly the low abundance microbe was affected. Interestingly, BVDV infection significantly reduced the diversity of gut microbiota and changed its composition in gut microbiota-dysbiosis mice. Furthermore, compared with normal mice of BVDV infection, there were more viral loads in the duodenum, jejunum, spleen, and liver of the gut microbiota-dysbiosis mice. However, feces microbiota transplantation (FMT) reversed these effects. The data above indicated that the dysbiosis of gut microbiota was a key factor in the high infection rate of BVDV. It is found that the IFN-I signal was involved by investigating the underlying mechanisms. The inhibition of the proliferation and increase in the apoptosis of peripheral blood lymphocytes (PBL) were also observed. However, FMT treatment reversed these changes by regulating PI3K/Akt, ERK, and Caspase-9/Caspase-3 pathways. Furthermore, the involvement of butyrate in the pathogenesis of BVDV was also further confirmed. Our results showed for the first time that gut microbiota acts as a key endogenous defense mechanism against BVDV infection; moreover, targeting regulation of gut microbiota structure and abundance may serve as a new strategy to prevent and control the disease.IMPORTANCEWhether the high infection rate of BVDV is related to gut microbiota has not been reported. In addition, most studies on BVDV focus on in vitro experiments, which limits the study of its prevention and control strategy and its pathogenic mechanism. In this study, we successfully confirmed the causal relationship between gut microbiota and BVDV infection as well as the potential molecular mechanism based on a mouse model of BVDV infection and a mouse model of gut microbiota dysbiosis. Meanwhile, a mouse model which is more susceptible to BVDV provided in this study lays an important foundation for further research on prevention and control strategy of BVDV and its pathogenesis. In addition, the antiviral effect of butyrate, the metabolites of butyrate-producing bacteria, has been further revealed. Overall, our findings provide a promising prevention and control strategy to treat this infectious disease which is distributed worldwide.

Fabrication of zein-tamarind seed polysaccharide-curcumin nanocomplexes: their characterization and impact on alleviating colitis and gut microbiota dysbiosis in mice.

In this work, a zein-tamarind seed polysaccharide (TSP) co-delivery system was fabricated using an anti-solvent precipitation method. The formation mechanism, characterization, and effect on alleviating colitis and gut microbiota dysbiosis in mice of zein-TSP-curcumin (Z/T-Cur) nanocomplexes were investigated. Hydrogen bonding and the hydrophobic effect played a key role in the formation of Z/T-Cur nanocomplexes, and the interactions were spontaneous and driven by enthalpy. The encapsulation efficiency, loading capacity, and bioavailability increased from 60.8% (Zein-Cur) to 91.7% (Z/T-Cur1:1), from 6.1% (Zein-Cur) to 18.3% (Z/T-Cur1:1), and from 4.7% (Zein-Cur) to 20.0% (Z/T-Cur1:1), respectively. The Z/T-Cur significantly alleviated colitis symptoms in DSS-treated mice. Additionally, the prepared nanocomplexes rebalanced the gut microbiota composition of colitis mice by increasing the abundance of Akkermansia. Odoribacter and Monoglobus were rich in the Z-T-Cur treatment group, and Turicibacter and Bifidobacterium were rich in the zein-TSP treatment group. This study demonstrated that the TSP could be helpful in the targeted drug delivery system.

Peimisine ameliorates DSS-induced colitis by suppressing Jak-Stat activation and alleviating gut microbiota dysbiosis in mice.

Inflammatory cytokine secretion and gut microbiota dysbiosis play crucial roles in ulcerative colitis. In this research, the protective effects of peimisine on colitis mice were investigated. The protective effects were evaluated by the disease activity index, colonic length, hematoxylin-eosin, and AB/PAS Staining. The protective mechanisms were analyzed by ELISA, Western-blot, immunohistochemistry staining, immunofluorescence staining, and 16S rRNA gene analysis. The results showed that peimisine treatment could reduce the disease activity index, prevent colonic shortening, and alleviate colon tissue damage. Peimisine treatment also decreased the levels of MCP-1, IL-1β, IL-6, IFN-γ, TNF-α and affected macrophage polarization and Th17/Treg cell balance by downregulating the expression of jak1/2, p-jak1/2, stat1/3, and p-stat1/3. Moreover, peimisine treatment significantly increased the abundances of beneficial microbes (e.g. Ruminococcaceae UCG-014 and Lachnospiraceae_NK4A136_group) and decreased the abundances of harmful microbes (e.g. Bacteroides and Escherichia). Peimisine can ameliorate colitis by inhibiting Jak-Stat signaling pathway, reversing gut microbiota alterations, suppressing macrophage M1 polarization, maintaining the Th17/Treg cell balance, and reducing sustained inflammatory cytokines-related inflammatory injury.

18. Ethanol-induced potentiation of post-burn neuroinflammation correlates with gut microbiota dysbiosis in mice

18. Ethanol-induced potentiation of post-burn neuroinflammation correlates with gut microbiota dysbiosis in mice

Pomelo peel dietary fiber ameliorates alterations in obesity-related features and gut microbiota dysbiosis in mice fed on a high-fat diet

Pomelo peel has abundance of dietary fiber and various biological activities but is often discarded as waste. This study evaluated the biological activities of pomelo peel dietary fiber (PPDF) in preventing obesity and regulating intestinal microbiota in obese mouse model induced using a high-fat diet (HFD). As for the composition, the prepared PPDF contained 89.64% of total dietary fiber, 53.27% of insoluble dietary fiber, and 36.37% of soluble dietary fiber. PPDF treatment significantly reduced weight gain and fat accumulation in the liver and epididymal tissues of obese mice; significantly alleviated HFD-induced dyslipidemia; and restored the levels of triglycerides, low-density lipoprotein–cholesterol, and high-density lipoprotein–-cholesterol to control levels, and the PPDF 5% dose restored total cholesterol to the control level. Furthermore, PPDF ameliorated HFD-induced gut microbiota dysbiosis by increasing intestinal microbial diversity, decreasing the Firmicutes/Bacteroidetes ratio, increasing beneficial bacteria (Bifidobacterium, Alloprevotella, and Lactobacillus), and decreasing harmful bacteria (Staphylococcus and Corynebacterium_1). This study provided a new idea to use PPDF as functional food to prevent obesity, alleviate dyslipidemia, or a potential probiotic to ameliorate gut microbiota dysbiosis.

Bifidobacterium lactis TY-S01 protects against alcoholic liver injury in mice by regulating intestinal barrier function and gut microbiota

Alcohol-induced liver injury poses a significant threat to human health. Probiotics have been proven to prevent and treat alcohol-induced liver injury. In this study, the preventive effect of Bifidobacterium lactis TY-S01 on alcohol-induced liver injury in mice was investigated. TY-S01 pretreatment effectively protected mice against alcohol-induced liver injury by preserving the levels of alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, triglyceride and high-density lipoprotein-cholesterol in serum and maintaining the levels of the inflammatory cytokines tumor necrosis factor-α, interleukin-6 and interleukin-1β in liver tissue. Additionally, TY-S01 could maintain the endotoxin levels in serum, maintain the mRNA expression levels of zonula occluden-1, occludin, claudin-1 and claudin-3 in the gut, and prevent gut microbiota dysbiosis in mice with alcoholic liver injury. Spearman's correlation analysis revealed that there was a clear correlation among serum indicators, inflammatory cytokines and gut microbiota. In conclusion, TY-S01 attenuates alcohol-induced liver injury by protecting the integrity of the intestinal barrier and maintaining the balance of the gut microbiota.

Chronic exposure to UVB induces nephritis and gut microbiota dysbiosis in mice based on the integration of renal transcriptome profiles and 16S rRNA sequencing data

Ultraviolet (UV) is a common and abundant environmental factor that affects daily life. Although the effects of UV radiation on the skin have been extensively reported, studies on the influence of UV radiation on internal organs are still limited. This study aimed to evaluate the influence of UVB exposure on the kidney of mice and to investigate the possible mechanism. In the present study, histopathology changes, oxidative stress, and inflammatory response were used to evaluate the kidney and colon injury induced by UVB exposure. The results showed that the 14-week chronic skin exposure to UVB triggers a kidney injury response characterized by macrophage infiltration, elevated oxidative stress as well as inflammatory and injury markers. The RNA sequencing demonstrated that chronic UVB exposure could alter the kidney transcriptomic profile distinguished by the regulation of genes involved in the Notch signaling pathway, JAK-STAT signaling pathway, and ECM-receptor interaction. Besides, chronic UVB exposure also resulted in gut dysbiosis, manifested as colon macrophage infiltration, stimulated inflammatory responses, impaired barrier integrity, and microbiota structural and functional disorders. The Spearman analysis results further revealed a strong correlation between gut microbiota and kidney injury. In conclusion, skin chronic exposure to UVB causes nephritis and gut microbiota dysbiosis in mice, and these findings provide new insight into the underlying risks of chronic UVB exposure to human wellness.

Foxtail millet (Setaria italica) alleviates non-alcoholic fatty liver disease in high-fat diet/streptozotocin-induced diabetic mice through gut microbiota modulation

Non-alcoholic fatty liver disease (NAFLD), caused by increased hepatic fat accumulation, inflammation, and oxidative stress, is one of the most common complications of diabetes. The hypoglycemic effect of foxtail millet supplementation has been studied previously. However, the influence of foxtail millet on diabetes-induced NAFLD remains unknown. The present study investigated the role of heat-treated foxtail millet (HFM) in alleviating NAFLD-related phenotypic indicators and altering gut composition in diabetic mice. Our disease model was established using a high-fat diet combined with streptozotocin before HFM supplementation. In diseased mice, the consumption of HFM reduced hepatic total cholesterol by 21.13%, triglyceride by 18.59%, malondialdehyde by 42.64%, and increased superoxide dismutase by 14.98% in the liver, respectively. Also, fasting blood glucose and serum insulin levels significantly decreased by 30.11% and 30.09%, respectively. 16S rRNA gene sequencing analysis indicated that HFM alleviated NAFLD-related gut microbiota dysbiosis in mice. Specifically, HFM treatment regulated gut microbiota composition, enriched probiotics (Bifidobacterium, Prevotellaceae_UCG-001, and Allobaculum), reduced harmful bacteria (Peptococcus, Oscillibacter, and Escherichia-Shigella), and elevated short-chain fatty acid concentrations. These findings demonstrated that the beneficial effects of HFM on NAFLD may be associated with changes in gut microbiota composition.

Geniposidic acid attenuates DSS-induced colitis through inhibiting inflammation and regulating gut microbiota.

Geniposidic acid (GPA) is a bioactive compound isolated from Gardenia jasminoides Ellis (Rubiaceae) that has long been used to treat arthritis, jaundice, and hypertension. However, the therapeutic effects of GPA against colitis remain underexplored. This study aimed to investigate the effect of GPA on the remission of colitis and the underlying mechanisms. A DSS-induced colitis mouse model was used to evaluate the influence of GPA on the modulation of gut microbiota and intestinal epithelial barrier function. Our results indicated that GPA improved DSS-induced mouse colitis, including loss of body weight, disease activity index (DAI), colon length, and colonic pathological damage. DSS-induced destruction of the intestinal barrier was also significantly repaired by GPA treatment. In addition, the relative levels of pro-inflammatory cytokines, such as IL-1β and TNF-α, were markedly alleviated by GPA. Furthermore, western blot analysis revealed that GPA downregulated the protein expression of the nuclear transcription factor NF-κB. Finally, we first demonstrated that GPA could alleviate gut microbiota dysbiosis in mice with colitis by bacterial 16S rRNA sequencing. In conclusion, our study demonstrates the therapeutic and protective effects of GPA on IBD and provides novel insights into the prevention of colitis by targeting gut microbiota metabolism using natural products.

Bisphenol P exposure in C57BL/6 mice caused gut microbiota dysbiosis and induced intestinal barrier disruption via LPS/TLR4/NF-κB signaling pathway

Despite being one of the most world's widely used and mass-produced compounds, bisphenol A (BPA) has a wide range of toxic effects. Bisphenol P (BPP), an alternative to BPA, has been detected in many foods. The effects of BPP dietary exposure on gut microbiota and the intestinal barrier were unclear. We designed three batches of animal experiments: The first studied mice were exposed to BPP (30 µg/kg BW/day) for nine weeks and found that they gained weight and developed dysbiosis of the gut microbiota. The second, using typical human exposure levels (L, 0.3 µg/kg BW/day BPP) and higher concentrations (M, 30 µg/kg BW/day BPP; H, 3000 µg/kg BW/day BPP), caused gut microbiota dysbiosis in mice, activated the Lipopolysaccharide (LPS) /TLR4/NF-κB signaling pathway, triggered an inflammatory response, increased intestinal permeability, and promoted bacterial translocation leading to intestinal barrier disruption. The third treatment used a combination of antibiotics and alleviated intestinal inflammation and injury. This study demonstrated the mechanism of injury and concentration effects of intestinal damage caused by BPP exposure, providing reference data for BPP use and control and yielding new insights for human disease prevention.

P2X4 receptor modulates gut inflammation and favours microbial homeostasis in colitis.

Inflammatory bowel disease (IBD) is a non-specific chronic inflammatory disease of the intestine. In addition to genetic susceptibility, environmental factorsand dysregulated host immunity, the gut microbiota is implicated in the pathogenesis of Crohn's disease (CD) or ulcerative colitis (UC), the two primary types of IBD. The P2X4 receptor has been demonstrated to have a crucial role in preventing infection, inflammation, and organ damage. However, it remains unclear whether the P2X4 receptor affects IBD and the underlying mechanisms. Colitis was induced in mice administrated with dextran sodium sulphate (DSS). 16S rDNA sequencing was used to analyze the gut microbiota in knockout and wild-type mice. Clinical and histopathological parameters were monitored throughout the disease progression. Gene Expression Omnibus analysis showed the downregulation of P2RX4 (P2rx4) expression in colonic tissues from patients or mice with IBD. However, its expression at the protein levels was upregulated on day 4 or 6 and then downregulated on day 7 in C57BL/6 mice treated with DSS. Gene ablation of P2rx4 aggravated DSS-induced colitis accompanying gut microbiota dysbiosis in mice. Moreover, P2X4 receptor-positive modulator ivermectin alleviated colitis and corrected dysregulated microbiota in wild-type C57BL/6 mice. Further antibiotic-treated gut microbiota depletion, cohousing experiment, and fecal microbiota transplantation proved that gut microbiota dysbiosis was associated with the aggravation of colitis in the mouse model initiated by P2rx4. Our findings elaborate on an unrevealed etiopathophysiological mechanism by which microbiota dysbiosis induced by the P2X4 receptor influences the development of colitis, indicating that the P2X4 receptor represents a promising target for treating patients with CD and UC.

Mechanochemical preparation of red clover extract/β-cyclodextrin dispersion: Enhanced water solubility and activities in alleviating high-fat diet-induced lipid accumulation and gut microbiota dysbiosis in mice

Red clover (RC) extract is rich in isoflavones (formononetin and biochanin A) that have various biological functions. However, its low water solubility limits its bioavailability. In this study, an RC extract/β-cyclodextrin (RC/β-CD) dispersion was prepared by ball milling to enhance its water solubility and biological availability. The water solubility of formononetin and biochanin A was 34.45 and 13.65 μg/mL (increased to 3.11 and 2.14 times higher than that of RC alone), respectively. The alleviating effects of the dispersion on lipid accumulation and gut microbiota were evaluated in mice. The RC/β-CD dispersion showed a better effect on inhibiting lipid accumulation, especially on total triglycerides. The dispersion group had a higher relative abundance of Akkermansia, Muribaculaceae, and Bacteroides than RC alone, along with a higher level of acetic and butyric acid. The study provides a feasible way for improving the bioaccessibility and bioactivity of RC isoflavones in red clover.

Dietary Turmeric Consumption Alleviates Ulcerative Colitis via Restoring Tryptophan Metabolism and Alleviating Gut Microbiota Dysbiosis in Mice.

This study was designed to first verify the protective capacity of turmeric powder (TP) as a traditional cooking spice against dextran sulfate sodium (DSS)-induced intestinal inflammation and intestine microbiota imbalance. The DSS-induced mice were fed a standard rodent chow supplemented with or without TP (8%) for 37 days. The results indicated that the pathological phenotype, gut barrier disruption, and colon inflammation of DSS-induced mice were significantly improved through supplementation of TP. In addition, 16S rRNA-based microbiota or targeted metabolomics analysis indicated that TP ameliorated intestinal microbiota dysbiosis caused by DSS and particularly enhanced the abundances of probiotics correlated with tryptophan metabolism, such as Lactobacillus and Bifidobacterium, where the cecal tryptophan was metabolized to indole-3-propionic acid and indole-3-acetic acid. Consumption of TP markedly enhanced the expression levels of colonic aromatic hydrocarbon receptors and further increased the expressions of intestinal tight junction proteins and interleukin-22 in the colitis mice. Collectively, these findings manifest the protective actions of dietary TP consumption against ulcerative colitis via restoring the intestinal microbiota disorders, promoting microbial metabolism, and improving intestinal barrier damage.

Effects of highland barley β-glucan on blood glucose and gut microbiota in streptozotocin-induced, diabetic, C57BL/6 mice on a high-fat diet

ObjectivesThis study aimed to investigate the hypoglycemic effect of highland barley β-glucan (HBG) on mice with type 2 diabetes (T2D), and determine whether the hypoglycemic effects are related to modulations of the gut microbiota. MethodsT2D was induced with a high-fat diet and streptozotocin in the mice. HBG was orally administered to mice with T2D for 4 wk, and biochemical indices were analyzed in the serum and liver. Fecal samples were collected and analyzed with high-throughput 16S ribosomal RNA sequencing. ResultsIntake of HBG for 4 wk suppressed the body weight, as well as liver and heart indices, and regulated the levels of fasting blood glucose, serum insulin, blood lipid, oxidative damage, and inflammatory reaction in mice with T2D. Furthermore, HBG reversed the gut microbiota dysbiosis in mice with T2D by increasing the abundance of Lachnospiraceae_UCG-006, Streptococcaceae, and Eggerthellaceae, and by decreasing the abundance of Parasutterella. ConclusionsOur findings indicate that the antidiabetic abilities of HBG might be related to the improvement of gut microbiota imbalance.

Lacticaseibacillus rhamnosus-Derived Exopolysaccharide Attenuates D-Galactose-Induced Oxidative Stress and Inflammatory Brain Injury and Modulates Gut Microbiota in a Mouse Model.

This study aimed to investigate the protective effect of a novel exopolysaccharide EPSRam12, produced by Lacticaseibacillus rhamnosus Ram12, against D-galactose-induced brain injury and gut microbiota dysbiosis in mice. The findings demonstrate that EPSRam12 increases the level of antioxidant enzymes superoxide dismutase, catalase and glutathione peroxidase, total antioxidant capacity, and the level of anti-inflammatory cytokine IL-10, while decreasing malonaldehyde, nitric oxide, pro-inflammatory cytokines including TNF-α, IL-1β, IL-6, MCP-1, and the mRNA expression of cyclooxygenase-2, inducible nitric oxide synthase, and the activation of nuclear factor-kappa-B in the brain tissues of D-galactose-treated mice. Further analyses reveal that EPSRam12 improves gut mucosal barrier function and increases the levels of short-chain fatty acids (SCFAs) in the intestine while restoring gut microbial diversity by enriching the abundance of SCFA-producing microbial genera Prevotella, Clostridium, Intestinimonas, and Acetatifactor while decreasing potential pathobionts including Helicobacter. These findings of antioxidative and anti-inflammatory effects in the brain and ameliorative effects on epithelial integrity, SCFAs and microbiota in the gut, provide novel insights into the effect of EPSRam12 intervention on the gut–microbiome–brain axis and should facilitate prospective understanding of microbial exopolysaccharide for improved host health.

Oyster Protein Hydrolysate Alleviates Cadmium Toxicity by Restoring Cadmium-Induced Intestinal Damage and Gut Microbiota Dysbiosis in Mice via Its Abundance of Methionine, Tyrosine, and Glutamine

Oyster Protein Hydrolysate Alleviates Cadmium Toxicity by Restoring Cadmium-Induced Intestinal Damage and Gut Microbiota Dysbiosis in Mice via Its Abundance of Methionine, Tyrosine, and Glutamine

Chronic exposure to polyvinyl chloride microplastics induces liver injury and gut microbiota dysbiosis based on the integration of liver transcriptome profiles and full-length 16S rRNA sequencing data

Microplastics (MPs) have become harmful environmental pollutants, and their potential toxicity to organisms has attracted extensive attention. However, the effects of polyvinyl chloride MPs (PVC-MPs) on the liver and their associated mechanism in mice remain obscure. Here, male mice were exposed to 2-μm PVC-MPs (0.5 mg/day) for 60 days and then sacrificed, and their liver, blood and gut feces were subsequently collected for testing. The liver tissue and fecal samples were subjected to RNA sequencing and full-length 16S rRNA sequencing analysis, respectively. Our results showed that the levels of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in the mice exposed to PVC-MPs were markedly higher than those in the control group, implying hepatic injury, as evidenced by hepatic histopathological changes. Moreover, the serum and hepatic triglyceride (TG) and total bile acid (TBA) levels were decreased after exposure to PVC-MPs. The RNA sequencing of mouse liver tissue identified a total of 1540 differentially expressed genes (DEGs) associated with 47 pathways, including the lipid metabolic pathway, oxidative stress, and the phosphoinositide 3 kinase (PI3K)/protein kinase B (Akt) signaling pathway, and these DEGs were enriched in the mouse livers. The full-length 16S rRNA sequencing analysis of the gut microbiota in mouse fecal samples revealed that PVC-MPs exposure decreased the relative abundance of probiotics and increased the abundance of conditionally pathogenic bacteria. In conclusion, chronic PVC-MPs exposure causes hepatotoxicity and gut microbiota dysbiosis in mice, and these findings provide new insight into the potential risks of PVC-MPs to human health.