Advanced Healthcare Materials
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2025
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IF 9.6
Nianhua Zhang,Xu Zhang,Jiulong Li,Baoyi Li,Shuai Wang,Xiao Liu,Huan Meng,Motao Zhu
While convenient for patient compliance, the efficacy of oral treatments for inflammatory bowel disease (IBD) is often compromised by the dynamic and harsh chemical environment of the gastrointestinal tract, presenting challenges for effective therapeutic management. The pathological complexity of IBD frequently involves multiple factors such as oxidative stress, immune dysregulation, gut microbiome abnormality, and inadequate drug bioavailability, among others. To address these challenges, this project develops an oral nanomedicine platform based on mesoporous silica nanoparticles with a cerium oxide core, further coated with an outer membrane (OM) derived from Akkermansia muciniphila ( Akk ), a beneficial bacteria naturally present in the human gut. This novel nanocomplex, termed “OM-CeMeso,” is evaluated for its enhanced stability, reactive oxygen species (ROS) scavenging capacity, and ability to restore microbiota homeostasis. This project demonstrates that the silica-based nanomaterials’ acid-resistant yet base-degradable properties significantly improved stability in a murine IBD model. The incorporation of cerium oxide nanoparticles (CeO 2 NPs) added further benefits by enhancing ROS scavenging. Notably, the Akk- derived OM coat also increases the diversity and abundance of beneficial gut microbiota. These complementary and integrated functions lead to significant symptom alleviation in murine IBD models while avoiding any unwanted toxicity.
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高影响因子
CARBOHYDRATE POLYMERS
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2025
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IF 12.5
Xiaoyu Wu,Jiajia Wei,Rongzheng Deng,Jinyu Wang,Bo Wu,Tingxu Yan,Ying Jia
Current therapies for ulcerative colitis (UC) remain inadequate, necessitating novel treatment strategies. This study isolated SCPII-1, a homogeneous pectin polysaccharide (Mw: 278.153 kDa, DM: 57.21 %) from Schisandra chinensis , primarily composed of →4)-α-D-GalpA-(1 → units. In dextran sulfate sodium (DSS)-induced colitis mice, SCPII-1 alleviated symptoms, repaired mucosal ultrastructure (microvilli, mitochondria), and enhanced barrier integrity. Mechanistically, SCPII-1 ameliorated gut dysbiosis in UC mice, notably through the selective enrichment of the beneficial bacterium Akkermansia muciniphila (AKK). Interestingly, SCPII-1 not only promoted the proliferation of AKK but also modulated its tryptophan metabolism, particularly enhancing the production of the tryptophan-derived metabolite indole-3-ethanol (I3E). The beneficial role of SCPII-1-induced microbiota in UC was validated using pseudo-germ-free mice and fecal microbiota transplantation experiments. Moreover, I3E was identified as a key microbiota-derived active metabolite regulated by SCPII-1, and exogenous supplementation of I3E further confirmed its therapeutic efficacy in UC. Importantly, I3E activated the aryl hydrocarbon receptor (AhR), upregulated IL-22 expression, and promoted mucosal repair and immune homeostasis, thereby confirming the protective role of the SCPII-1-AKK-tryptophan metabolism axis in colitis. These findings highlight SCPII-1 as a promising prebiotic agent for UC treatment by modulating AKK-dependent tryptophan metabolism and activating the AhR/IL-22 signaling pathway, offering a novel microbiota-based therapeutic strategy.
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高影响因子
GLYCOCONJUGATE JOURNAL
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2018
·Vol. 35
·期 3
·255-263
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IF 2.548
Guo Bi-Shan,Zheng Feng,Crouch Lucy,Cai Zhi-Peng,Wang Meng,Bolam David N.,Liu Li,Voglmeir Josef
A putative GH35 β-galactosidase gene from the mucin-degrading bacterium Akkermansia muciniphila was successfully cloned and further investigated. The recombinant enzyme with the molecular mass of 74 kDa was purified to homogeneity and biochemically characterised. The optimum temperature of the enzyme was 42 °C, and the optimum pH was determined to be pH 3.5. The addition of sodium dodecyl sulphate (SDS) reduced the enzyme’s activity significantly. The addition of Mg 2+ -ions decreased the activity of the β-galactosidase, whereas other metal ions or EDTA showed no inhibitory effect. The enzyme catalysed the hydrolysis of β1,3- and β1,6- linked galactose residues from various substrates, whereas only negligible amounts of β1,4-galactose were hydrolysed. The present study describes the first functional characterisation of a β-galactosidase from this human gut symbiont.
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高影响因子
Frontiers in Microbiology
·
2026
·
IF 5.8
Mengting Li,Shuiming Xiao,Yanli Wang,Tao Li,Qin Hu,Lijinchuan Dong,Yuxuan Guo,Zhe Shi,Qing Yang,Weiyan Cai,Qi Li,Bo Peng,Pengyue Li,Xiaogang Weng,Yajie Wang,Yujie Li,Yu Dong,Xiaoxin Zhu,Zipeng Gong,Ying Chen
Introduction Irritable bowel syndrome (IBS) is a typical disorder of gut-brain interaction (DGBI). The microbiota-gut-brain (MGB) axis is pivotal in preventing and treating IBS. Wuji Pill is a traditional Chinese medicine commonly used to treat IBS. This study aimed to investigate the mechanism by which Wuji Pill improves IBS via the MGB axis. Methods The visceral sensitivity and colonic motor function were evaluated using the abdominal wall withdrawal reflex test and the colonic motility curve. Depression-like behavior were evaluated using sucrose preference test, open field test, novelty-suppressed feeding test, and forced swimming tests. The intestinal mucus secretion and the activation status of microglia was detected using AB-PAS staining and immunofluorescence staining, respectively. The species composition and abundance of gut microbiota were detected through 16S rRNA sequencing and RT-qPCR. Targeted metabonomics and RT-qPCR were used for metabolites and metabolic enzymes analysis. Results In this study, Wuji Pill improved the symptoms of IBS rats and increased the relative abundance of Akkermansia muciniphila in feces. Additionally, antibiotics affected the repair of intestinal mucus secretion and significantly reduced the level of short-chain fatty acids. Subsequently, fecal microbiota transplantation and A. muciniphila transplantation can improve the symptoms of IBS rat by increasing intestinal mucus secretion, elevating the levels of acetic acid and butyric acid in feces. Additionally, the microglia in the cortex were suppressed, and the tryptophan-kynurenine pathway in the hippocampus was inhibited, leading to the conversion of tryptophan into 5-HT. Discussion This study highlights the Wuji Pill may alleviate IBS symptoms by modulating A. muciniphila and regulating the tryptophan metabolism pathway through MGB axis.
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高影响因子
PHYTOMEDICINE
·
2022
·
IF 6.656
Zichen Luo,Weichen Xu,Tianjie Yuan,Chen Shi,Tianzi Jin,Ying Chong,Jianjian Ji,Lili Lin,Jianya Xu,Ying Zhang,An Kang,Wei Zhou,Tong Xie,Liuqing Di,Jinjun Shan
Background Increasing hepatic insulin signaling is found to be an important mechanism of Platycodon grandiflorus root to alleviate metabolic syndrome (MetS) symptoms such as insulin resistance, obesity, hyperlipidemia and hepatic steatosis , but the details are not yet clear. Since the main constituents of Platycodon grandiflorus root were hard to be absorbed by gastrointestinal tract , getting opportunity to interact with gut microbiota , we speculate the gut microorganisms may mediate its effect. Purpose Our work aimed to confirm the critical role of gut microbes in the intervention of Platycodon grandiflorus root extract (PRE) on MetS, and investigate the mechanism. Methods Biochemical analyses, glucose tolerance test and hepatic lipidomics analysis were used to evaluate the anti-MetS effect of PRE on high fat diet (HFD) fed mice. Perform 16S rDNA analysis, qPCR analysis and in vitro co-incubation experiment to study its effect on gut microbes, followed by fecal microbiota transplantation (FMT) experiment and antibiotics intervention experiment. Also, the effect of Akkermansia muciniphila treatment on HFD mice was investigated. Results PRE alleviated lipid accumulation and insulin resistance in HFD mice and remodeled the fecal microbiome . It also increased the gene expression of colonic tight junction proteins , alleviated metabolic endotoxemia and inflammation, so that reduced TNF-α induced hepatic JNK-dependent IRS-1 serine phosphorylation and the impairment of PI3K/PIP3/Akt insulin signaling pathway. A. muciniphila was one of the most significantly enriched microbes by PRE treatment, and its administration to HFD mice showed similar effects to PRE, repairing the gut barrier and activating hepatic PI3K/PIP3/Akt pathway. Finally, anti-MetS effect of PRE could be delivered to FMT recipients, and PRE could not further attenuate MetS in gut microbiota depleted mice. Conclusion We demonstrated for the first time that PRE alleviated MetS in a gut microbiota dependent manner, and found activation of hepatic insulin signaling mediated by gut A. muciniphila was a potential mechanism of it.
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Frontiers in Microbiology
·
2026
·
IF 5.8
Huilin Yang,Shuai Liu,Xia Chen,Chenxi Yin,Longxia Xiao,Wenmin Xu,Shuaijun Lv,Li Xie,Chunhua Yin
BackgroundEndometriosis (EMs) is a chronic inflammatory disease characterized by tumor-like growth behavior and limited therapeutic options. Increasing evidence suggests that gut microbiota may contribute to EMs progression by promoting chronic inflammation and immune dysregulation. Fluvastatin, a lipid-lowering agent, exhibits anti-inflammatory, anti-tumor, and immunomodulatory effects and has also been reported to influence microbial homeostasis. However, the relationship among fluvastatin treatment, gut microbiota, and EMs progression remains unclear. This study aimed to investigate this relationship.Materials and methodsA mouse model of EMs was established by autologous uterine tissue transplantation, followed by oral fluvastatin administration for 3 weeks. Lesion growth, inflammatory responses, and immune characteristics were evaluated by histology, quantitative PCR, flow cytometry, immunofluorescence, and immunohistochemistry. Gut microbiota involvement was assessed using antibiotic-mediated microbiota depletion and fecal microbiota transplantation (FMT). Microbial composition was analyzed by metagenomic sequencing. The role of Akkermansia muciniphila was evaluated by direct oral supplementation.ResultsFluvastatin significantly reduced the volume and mass of ectopic lesions and decreased the mRNA expression of pro-inflammatory cytokines. It was also associated with changes in macrophage polarization-related markers and reduced abnormal activation of splenic immune cells. Antibiotic-induced gut microbiota depletion attenuated the protective effects associated with fluvastatin treatment, whereas FMT from fluvastatin-treated mice partially transferred similar protective changes. Metagenomic analysis revealed that fluvastatin reshaped gut microbiota composition and increased the abundance of Akkermansia muciniphila. Moreover, oral supplementation with Akkermansia muciniphila attenuated EMs progression and was associated with anti-inflammatory and immune-related changes similar to those observed after fluvastatin treatment.ConclusionThese findings suggest that the protective effects associated with fluvastatin treatment are accompanied by changes in gut microbiota composition, including increased abundance of Akkermansia muciniphila. Gut microbiota may contribute to the beneficial effects of fluvastatin in EMs. These results support the potential value of microbiota-informed therapeutic strategies for EMs.
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