CARBOHYDRATE POLYMERS
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2025
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IF 12.5
Qianyun Zhao,Yubin Liu,Mingxing Li,Long Zhao,Tiangang Wang,Yaqin Xiao,Shulin Wei,Ke Wu,Jiayue Yang,Yaqiu Wang,Yueshui Zhao,Fukuan Du,Yu Chen,Shuai Deng,Jing Shen,Zhangang Xiao,Zhi Li,Shengpeng Wang,Xu Wu
Hawthorn fruit is rich in pectins; however, the gut microbiota-modulating effects of hawthorn pectin remain unclear. In this study, enzyme-extracted hawthorn pectin ( M w : 126.24 kDa; HG/RG-I ratio: 55.64 %/37.93 %; branching degree: 2.44) was fractionated into two components: D1 (spherical, 345.76 kDa, HG/RG-I 57.48 %/37.25 %, branching degree 2.16) and D2 (flexible, 17.20 kDa, HG/RG-I 78.24 %/21.76 %, branching degree 1.33). Hawthorn pectin directly stimulated Dubosiella newyorkensis and Bifidobacterium bifidum growth in vitro . In hyperlipidemic mice, it alleviated dyslipidemia and enriched Lactobacillus and Dubosiella . Parallel experiments confirmed that D. newyorkensis supplementation similarly reduced dyslipidemia and enhanced Lactobacillus abundance, mediated by bacterial acetate production. Only D1 mimicked the pectin's prebiotic activity, promoting D. newyorkensis and B. bifidum growth. The high-RG-I D1, with elevated branching and larger M w , was identified as the key driver of hawthorn pectin's prebiotic effect. These findings highlight that hawthorn pectin and D1 specifically target probiotic D. newyorkensis to synergize with Lactobacillus against hyperlipidemia.
研究领域:
营养学
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微生物学
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代谢疾病研究
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Cell Reports
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2025
·
IF 6.9
Tingting Xu,Dan Fang,Tianqi Xu,Xiuying Tao,Zhiqiang Wang,Yuan Liu
Gut microbiota plays a crucial role in resisting the invasion of pathogens, particularly multidrug-resistant (MDR) bacteria, which pose a significant threat to public health. While exercise offers numerous health benefits, its impact on host colonization resistance remains largely unclear. In this study, we demonstrate that moderate exercise significantly reduces gut colonization by methicillin-resistant Staphylococcus aureus (MRSA), a clinically important MDR pathogen. Moreover, we identify an understudied strain of the intestinal probiotic Dubosiella newyorkensis (L8) as a critical factor in mediating exercise-induced colonization resistance against MRSA. Mechanistically, L8 enhances the deprivation of fucose, a crucial carbon source essential for MRSA growth and pathogenicity. This process relies on the high binding affinity of pyruvate to the ILE257 site of the lactate dehydrogenase in L8. Overall, our work highlights the importance of moderate exercise in maintaining host colonization resistance and demonstrates L8 as a probiotic in protecting against MRSA colonization.
研究领域:
微生物学
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医学
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免疫学
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PubMed
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JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
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2026
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IF 6.7
Xinyu Cheng,Yifan Lei,Shuyang Zhang,Liping Chen,Yongzhong Wang
Hyperuricemia (HUA), a metabolic disorder resulting from disrupted uric acid (UA) homeostasis, is the principal etiological factor for gout. This study investigated the therapeutic potential of gut microbiota modulation in HUA using antibiotic-treated mouse models with butyrate intervention. Selective antibiotic screening identified the Dubosiella-type strain Dubosiella newyorkensis (Dn) as an effective intervention for HUA. Dn treatment significantly reduced UA production, improved renal function markers, and decreased oxidative stress. Dn enriches Bacteroides and Romboutsia while suppressing the pathobiont Thomasclavelia, thereby enhancing the production of acetate, propionate, and butyrate. Molecular analyses demonstrated that Dn downregulated the expression of URAT1 while upregulating ABCG2, thereby promoting UA excretion. Histopathological evaluation confirmed that Dn restored the glomerular atrophy, tubular dilation, and collagen deposition induced by HUA. These findings suggest that Dn is a promising multitarget therapeutic agent for HUA and provides a scientific foundation for the development of novel microbiome-based strategies against HUA.
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高影响因子
Biology-Basel
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2026
·Vol. 15
·期 13
·1030
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IF 4.3
Jin Li,Shirui Cheng,Wenqi Zhang,Shourong Qiao,Luzhi Zhang,Mengxu Yao,Yunxia Zhang,Biao Wang,Changjing Wu
Simple SummaryAlzheimer’s disease is a progressive neurodegenerative disorder that causes memory loss, cognitive decline, and great burden on patients and families. Although many studies have focused on the brain, increasing evidence suggests that changes in the gut may also contribute to disease development. In this study, we examined whether mulberroside A, a natural compound derived from mulberry, could protect against scopolamine-induced Alzheimer’s disease-like cognitive impairment in mice. Our results showed that mulberroside A improved learning and memory, reduced inflammatory damage and oxidative stress in the brain, and protected the intestinal barrier. We also found that mulberroside A changed the composition of gut microbes, especially increasing beneficial bacteria such asDubosiella, and helped restore abnormal metabolism in the brain. Importantly, fecal microbiota transplantation from treated mice reproduced the protective effects, indicating that gut microbiota changes play a key role in the action of mulberroside A. These findings suggest that mulberroside A may improve brain health by acting through the microbiota-gut–brain axis and could be a promising natural compound for the prevention and amelioration of Alzheimer’s disease-like cognitive decline.Mulberroside A (MsA) possesses neuroprotective effects, but whether it alleviates Alzheimer’s disease (AD)-like cognitive impairment through the microbiota–gut–brain axis remains unclear. Using a scopolamine-induced mouse model of acute cognitive impairment (male ICR mice,n= 10/group), we demonstrated that daily administration of MsA (10, 20, and 30 mg/kg/day) for 5 weeks significantly ameliorated cognitive performance in novel object recognition and Morris water maze tests. At the optimal dose (30 mg/kg/day), MsA suppressed hippocampal microglial activation, reduced pro-inflammatory cytokines (IL-6, IL-1β, TNF-α), and attenuated oxidative stress by decreasing malondialdehyde (MDA) while restoring superoxide dismutase (SOD) and glutathione (GSH) levels. MsA also strengthened intestinal barrier integrity (ZO-1, occludin) and significantly altered the gut microbiota, notably increasing the beneficial genusDubosiella. Brain metabolomics indicated that MsA reversed scopolamine-induced metabolic disturbances, mainly restoring phospholipid balance. Correlation analysis demonstrated a strong gut–brain connection, withDubosiellaabundance positively associated with neuroprotective phospholipids and negatively with stress markers. Furthermore, fecal microbiota transplantation from MsA-treated donors successfully replicated these behavioral improvements in recipient mice, underscoring the functional involvement of the reshaped microbiome rather than a simple autonomous recovery. These results suggest that MsA alleviates AD-like cognitive impairment by reducing neuroinflammation and oxidative stress through microbiota remodeling, enhancing the intestinal barrier, and modulating theDubosiella-associated gut–metabolite–brain axis, making MsA a promising multi-target nutraceutical for ameliorating AD-like cognitive deficits.
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Microbiology Spectrum
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2024
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IF 3.7
Yvhao Xie,Xinxin Li,Qingshi Meng,Jinjun Li,Xin Wang,Liying Zhu,Weiwei Wang,Xiaoqiong Li
Tryptophan (TRP) metabolites have been identified as potent biomarkers for complications of type 2 diabetes mellitus (T2DM). However, it remains unclear whether the therapeutic effect of metformin in T2DM is related to the modulation of TRP metabolic pathway. This study aims to investigate whether metformin affects TRP metabolism in T2DM mice through the gut microbiota. A liquid chromatography-tandem mass spectrometry method was established to determine 16 TRP metabolites in the serum, colon content, urine, and feces of T2DM mice, and the correlations between metabolites and the T2DM mice gut microbiota were performed. The method demonstrated acceptable linearity (R2 > 0.996), with the limit of quantification ranging from 0.29 to 69.444 nmol/L for 16 analytes, and the limit of detection ranging from 0.087 to 20.833 nmol/L. In T2DM mice, metformin treatment effectively restored levels of indole-3-lactic acid (ILA), indole-3-propionic acid (IPA), and the ILA/IPA ratio, along with several aryl hydrocarbon receptor ligands in the serum, with a notable impact in the colon but not in the urine. This restoration was accompanied by a shift in the relative abundance of Dubosiella, Turicibacter, RF39, Clostridia_UCG-014, and Alistipes. Spearman’s correlation analysis revealed positive correlations between Turicibacter and Alistipes with IPA and indole-3-acetic acid. Conversely, these genera displayed negative correlations with ILA and kynurenine. In addition, our study revealed the presence of endogenous indole pathway in germ-free mice, and the impact of metformin on endogenous TRP metabolism in T2DM mice cannot be disregarded. Further research is needed to investigate the regulation of TRP metabolism by metformin.
研究领域:
药理学
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微生物学
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代谢组学
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糖尿病研究
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分子生物学
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