Changes In Microbiota Research Articles

Portocaval shunts' role in gut microbiota and hepatic encephalopathy: The gut-to-brain pathway

I read the study by Zhao et al with great interest. Although the study design was quite complicated, it was successful in raising awareness of science and relevant researchers. Thirty patients with liver cirrhosis and portal hypertension secondary to chronic hepatitis B were included in the study. They were treated for variceal bleeding and underwent trans-jugular intrahepatic portosystemic shunt to prevent the recurrence of variceal bleeding and to reduce portal pressure. The authors evaluated the effects of changes in gut microbiota (GM) on hepatic encephalopathy secondary to portocaval bypass. The GM is greatly affected by local and general factors, including herbal and medical drugs, a person's dietary characteristics (carnivorous, vegan, vegetarian), supplementary foods, drinking water sources, and living in a city center or town. Therefore, I congratulate Zhao et al for their concise and comprehensive study on a multifactorial subject.

Characteristic alterations of gut microbiota and serum metabolites in patients with chronic tinnitus: a multi-omics analysis

ABSTRACT Chronic tinnitus is a central nervous system disorder. Currently, the effects of gut microbiota on tinnitus remain unexplored. To explore the connection between gut microbiota and tinnitus, we conducted 16S rRNA sequencing of fecal microbiota and serum metabolomic analysis in a cohort of 70 patients with tinnitus and 30 healthy volunteers. We used the weighted gene co-expression network method to analyze the relationship between the gut microbiota and the serum metabolites. The random forest technique was utilized to select metabolites and gut taxa to construct predictive models. A pronounced gut dysbiosis in the tinnitus group, characterized by reduced bacterial diversity, an increased Firmicutes/Bacteroidetes ratio, and some opportunistic bacteria including Aeromonas and Acinetobacter were enriched. In contrast, some beneficial gut probiotics decreased, including Lactobacillales and Lactobacillaceae. In serum metabolomic analysis, serum metabolic disturbances in tinnitus patients and these differential metabolites were enriched in pathways of neuroinflammation, neurotransmitter activity, and synaptic function. The predictive models exhibited great diagnostic performance, achieving 0.94 (95% CI: 0.85–0.98) and 0.96 (95% CI: 0.86–0.99) in the test set. Our study suggests that changes in gut microbiota could potentially influence the occurrence and chronicity of tinnitus, and exert regulatory effects through changes in serum metabolites. Overall, this research provides new perceptions into the potential role of gut microbiota and serum metabolite in the pathogenesis of tinnitus, and proposes the “gut-brain-ear” concept as a pathomechanism underlying tinnitus, with significant clinical diagnostic implications and therapeutic potential. IMPORTANCE Tinnitus affects millions of people worldwide. Severe cases may lead to sleep disorders, anxiety, and depression, subsequently impacting patients’ lives and increasing societal healthcare expenditures. However, tinnitus mechanisms are poorly understood, and effective therapeutic interventions are currently lacking. We discovered the gut microbiota and serum metabolomics changes in patients with tinnitus, and provided the potential pathological mechanisms of dysregulated gut flora in chronic tinnitus. We proposed the innovative concept of the “gut-brain-ear axis,” which underscores the exploration of gut microbiota impact on susceptibility to chronic tinnitus through serum metabolic profile modulation. We also reveal novel biomarkers associated with chronic tinnitus, offering a new conceptual framework for further investigations into the susceptibility of patients, potential treatment targets for tinnitus, and assessing patient prognosis. Subsequently, gut microbiota and serum metabolites can be used as molecular markers to assess the susceptibility and prognosis of tinnitus.Furthermore, fecal transplantation may be used to treat tinnitus.

Weizmannia coagulans BC99 affects valeric acid production via regulating gut microbiota to ameliorate inflammation and oxidative stress responses in Helicobacter pylori mice

AbstractHelicobacter pylori is a highly prevalent pathogen in human gastric mucosa epithelial cells with strong colonization ability. Weizmannia coagulans is a kind of active microorganism that is beneficial to the improvement of host gut microbiota balance and can prevent and treat intestinal diseases. We investigated the beneficial effects of W. coagulans BC99 in H. pylori infected mice and measured inflammation response, oxidative stress, and gut microbiota. Results showed that BC99 could alleviate the gastric inflammation, inhibit the increasing of inflammation parameters endotoxin, interleukin‐10, transforming growth factor‐β, and interferon‐γ and oxidative stress myeloperoxidase and malondialdehyde, promote the levels of superoxide dismutase and catalase. Furthermore, 16S rRNA gene sequencing analysis revealed that BC99 reversed the change of gut microbiota by reducing the abundance of Olsenella, Candidatus_Saccharimonas, Monoglobus, and increasing the abundance of Tyzzerella. Meanwhile, BC99 caused elevated levels of Ligilactobacillus and Lactobacillus. In view of the beneficial effect of BC99 on the content of short‐chain fatty acid, valeric acid with sodium valerate interfered with H. pylori infection in mice found that valeric acid had a good restorative effect of H. pylori infection relating inflammation and oxidative stress responses. These results suggest that W. coagulans BC99 can be used as a potential probiotic to prevent and treat H. pylori infection by regulating the inflammation, oxidative stress, and gut microbiota.

Freeze-dried fecal microorganisms as an effective biomaterial for the treatment of calves suffering from diarrhea.

Fecal microbiota transplantation (FMT) is a therapeutic modality for treating neonatal calf diarrhea. Several practical barriers, including donor selection, fecal collection, and a limited timeframe for FMT, are the main constraints to using fresh feces for implementing on-farm FMT. We report the utility of FMT with pretreated ready-to-use frozen (F) or freeze-dried (FD) microorganisms for treating calf diarrhea. In total, 19 FMT (F-FMT, n = 10 and FD-FMT, n = 9) treatments were conducted. Both FMT treatments were 100% clinically effective; however, multi-omics analysis showed that FD-FMT was superior to F-FMT. Machine learning analysis with SourceTracker confirmed that donor microbiota was retained four times better in the recipient calves treated with FD-FMT than F-FMT. A predictive model based on receiver operating characteristic curve analysis and area under the curve showed that FD-FMT was more discriminative than F-FMT of the observed changes in microbiota and metabolites during disease recovery. These results provide new insights into establishing methods for preparing fecal microorganisms to increase the quality of FMT in animals and may contribute to FMT in humans.

The healing process of diabetic ulcers correlates with changes in the cutaneous microbiota.

Skin microbiota plays an essential role in the development and function of the cutaneous immune system, in the maintenance of the skin barrier through the release of antimicrobial peptides, and in the metabolism of some natural products. With the aim of characterizing changes in the cutaneous microbiota specifically associated with wound healing in the diabetic condition, we performed a 16S rRNA gene Next Generation Sequencing of skin swabs taken within the ulcer bed of ten diabetic patients before (t0) and after 20 days of therapy (t20) with a fluorescein-based galenic treatment. Considering the twenty most representative genera, we found at t20 an increase of Corynebacterium, Peptostreptococcus, and Streptococcus, and a decrease of Enterococcus, Finegoldia, and Peptoniphilus genera. However, differences were not significant due to the high variability among samples and the small patient cohort. S. aureus was the most abundant species at t0 and was reduced by therapy in four patients. Comparing the microbiome in the ulcer bed and in the perilesional tissue of the same patient at t0, no major differences were observed. Taken together, our data indicate that in the absence of antibiotic-based therapy the healing process of diabetic ulcers is accompanied by changes in the microbiome composition.

Abstract 4113494: Gut Microbiota Modulation by Immunosuppression and Cardiac Cell Therapy in a Nonhuman Primate Ischemia/Reperfusion Model of Cardiac Regeneration

End-stage ischemic heart disease necessitates heart transplantation, and emerging cell therapy presents a promising solution to address donor scarcity. Disruption of gut microbiota significantly influences various diseases and treatments, including transplantation. However, the impact of immunosuppression and cardiac cell therapy on gut microbiota remains largely unexplored. To elucidate this relationship, we investigated gut microbiota dynamics in response to immunosuppression and cell therapy in a nonhuman primate (NHP) cardiac ischemia/reperfusion (IR) model, with controlled genetic, dietary, and environmental factors. Immunosuppression enriched anaerobes (Faecalibacterium, Streptococcus, Anaerovibrio, Dialister), increasing gut microbiota diversity. These changes correlated with metabolic shifts towards amino acid metabolism and nucleosides/nucleotides biosynthesis. Combined treatment of human induced pluripotent stem cell (iPSC)-derived endothelial cells (EC) and cardiomyocytes (CM) also increased gut microbiota diversity, with specific genera alterations. The EC/CM co-treatment group displayed gut microbiota resembling the pre-injury group, with host metabolism shifting towards amino acid and fatty acid/lipid biosynthesis post-cell therapy. These observed microbiota changes and metabolic shifts could serve as biomarkers for monitoring cell therapy and immunosuppression outcomes, offering potential therapeutic targets to enhance efficacy.

Parkinson's Disease and the Microbiota-Gut-Brain Axis: Metabolites, Mechanisms, and Innovative Therapeutic Strategies Targeting the Gut Microbiota.

The human gut microbiota is diverse and abundant and plays important roles in regulating health by participating in metabolism and controlling physiological activities. The gut microbiota and its metabolites have been shown to affect the functioning of the gut and central nervous system through the microbiota-gut-brain axis. It is well established that microbiota play significant roles in the pathogenesis and progression of Parkinson's disease (PD). Disorders of the intestinal microbiota and altered metabolite levels are closely associated with PD. Here, the changes in intestinal microbiota and effects of metabolites in patients with PD are reviewed. Potential mechanisms underlying intestinal microbiota disorders in the pathogenesis of PD are briefly discussed. Additionally, we outline the current strategies for the treatment of PD that target the gut microbiota, emphasizing the development of promising novel strategies.

Intergenerational crosstalk of brain-gut axis in parental Nd2O3 exposure-induced offspring neurotoxicity and cognitive dysfunction: a mechanistic study

IntroductionRare earth elements (REEs) are widely used in plenty of fields. REEs have significant neurotoxicity and it may adversely affect the development of cognitive. For example, neodymium will causing neurological damage through penetrate the blood–brain barrier (BBB). However, whether it disrupts the balance of brain-gut axis (BGA) crosstalk and affects the intestinal microecology disorder of host is still unclear. This study investigated the neural damage on children caused by maternal exposure to Neodymium oxide (Nd2O3) during pregnancy, and its involved mechanism of BGA injury.MethodsWe used rat model to investigated the mechanisms of the offspring’s neural damage that Nd2O3 exposure in pregnancy. To verify the neural damage of offspring rats, we examed BBB-related factors, such like glutamate and ROS levels in brain tissue, behavioral tests, hippocampal and cortical damage, as well as changes in gut microbiota, intestinal mucosal barrier, and SCFAs in the intestine. Also, we observed some specific indicators of intestinal immune barrier function and gut nerve-related indicators.ResultsMaternal Nd2O3 exposure reduced the content of offspring tight junction proteins, increased BBB permeability, leading to Nd accumulation and brain tissue inflammation, affecting offspring’s neural development and weakening their spatial learning ability. Nd2O3 also disrupted BBB integrity by regulating SCFAs and BGA. Probiotic intervention in the offspring rats exposed to 2% Nd2O3 showed significant recovery of inflammation in both brain and colon tissues, and reduced BBB permeability.ConclusionMaternal exposure to Nd2O3 affects the offspring’s BGA, targeting brain and colon tissues, increasing BBB permeability, affecting neural development, causing damage to the intestinal mucosa, and impacting children’s gut development. Probiotics can alleviate these effects. These findings provide valuable insights into understanding the neurodevelopmental and intestinal developmental toxicity of Nd2O3 and its prevention and treatment. It also calls for a comprehensive assessment of the health risks of susceptible populations to Nd2O3, such as pregnant women. It may providing theoretical basis for preventing and controlling neodymium-induced harm in children by examing the repair mechanism of the damage through probiotic intervention.

Assessing functional properties of diet protein hydrolysate and oil from fish waste on canine immune parameters, cardiac biomarkers, and fecal microbiota

Locally produced fish hydrolysate and oil from the agrifood sector comprises a sustainable solution both to the problem of fish waste disposal and to the petfood sector with potential benefits for the animal’s health. This study evaluated the effects of the dietary replacement of mainly imported shrimp hydrolysate (5%) and salmon oil (3%; control diet) with locally produced fish hydrolysate (5%) and oil (3.2%) obtained from fish waste (experimental diet) on systemic inflammation markers, adipokines levels, cardiac function and fecal microbiota of adult dogs. Samples and measurements were taken from a feeding trial conducted according to a crossover design with two diets (control and experimental diets), six adult Beagle dogs per diet and two periods of 6 weeks each. The experimental diet, with higher docosahexaenoic (DHA) and eicosapentaenoic (EPA) acids contents, decreased plasmatic triglycerides and the activity of angiotensin converting enzyme, also tending to decrease total cholesterol. No effects of diet were observed on serum levels of the pro-inflammatory cytokines interleukin (IL)-1β, IL-8, and IL-12/IL-23 p40, and of the serum levels of the anti-inflammatory adipokine adiponectin. Blood pressure, heart rate and echocardiographic measurements were similar between diets with the only exception of left atrial to aorta diameter ratio that was higher in dogs fed the experimental diet, but without clinical relevance. Diet did not significantly affect fecal immunoglobulin A concentration. Regarding fecal microbiome, Megasphaera was the most abundant genus, followed by Bifidobacterium, Fusobacterium, and Prevotella, being the relative abundances of Fusobacterium and Ileibacterium genera positively affected by the experimental diet. Overall, results from the performed short term trial suggest that shrimp hydrolysate and salmon oil can be replaced by protein hydrolysate and oil from fish by-products without affecting systemic inflammatory markers, cardiac structure and function, but potentially benefiting bacterial genera associated with healthy microbiome. Considering the high DHA and EPA contents and the antioxidant properties of fish oil and hydrolysate, it would be worthwhile in the future to assess their long-term effects on inflammatory markers and their role in spontaneous canine cardiac diseases and to perform metabolomic and metagenomics analysis to elucidate the relevance of microbiota changes in the gut.

Effects of L-arginine on gut microbiota and muscle metabolism in fattening pigs based on omics analysis

IntroductionL-arginine is an α-amino acid and a semi-essential nutrient of significant biological interest. It plays a role in influencing various aspects of animal meat traits, gut microbiota composition, and physiological metabolism.MethodsThis study aimed to investigate the combined effects of L-arginine supplementation on gut microbiota composition and the metabolism of the longissimus dorsi muscle in fattening pigs. Eighteen Yorkshire commercial pigs were divided into two groups: a control group that received no supplements and a treatment group that was given 1% L-arginine for 52 days. The diversity and composition of microorganisms in the feces of the control (NC) and L-arginine (Arg) groups were analyzed by sequencing the 16S rRNA V3 -V4 region of the bacterial genome.ResultsThe findings indicated that L-arginine supplementation increased both the abundance and diversity of gut microbiota, particularly affecting the Firmicutes and Bacteroidetes phyla. KEGG enrichment analysis revealed significant changes in several metabolism-related pathways, including amino acid, carbohydrate, and lipid metabolism. Metabolomic analysis identified 85 differential metabolites between the arginine and control groups, with phospholipids ranking among the top 20. Additionally, functional predictions indicated an increased abundance in the glycerophospholipid metabolism pathway. Correlation analysis linked changes in gut microbiota to phospholipid levels, which subsequently influenced post-slaughter meat color and drip loss.DiscussionThese results suggest that L-arginine supplementation positively impacts gut microbiota composition and the metabolic profile of the longissimus dorsi muscle in fattening pigs, with potential implications for meat quality.

Cecal Microbial Diversity and Metabolome Reveal a Reduction in Growth Due to Oxidative Stress Caused by a Low-Energy Diet in Donkeys

Dietary energy level plays an important role in animal growth and development. The present study investigated the effect of dietary energy on the growth performance, antioxidative state, and nutrient digestion of meat donkeys. It simultaneously explored the probable reason for cecal microbiota and metabolome. Twelve meat donkeys (male) aged 1 year with a similar weight (150 ± 25 kg) were divided into two treatment groups: low-energy group (E1) and high-energy group (E2). The experiment was divided into a 10-day pre-trial period and a 135-day trial period. Donkeys in the trial periods were fed diets with digestible energy values (in dry matter) of 12.08 and 13.38 MJ/kg (pre-fattening, 1–45 d), 13.01 and 14.07 MJ/kg (mid-fattening, 46–90 d), and 13.54 and 14.93 MJ/kg (late-fattening, 91–135 d). The results show that E1 decreases body weight, average daily gain (ADG), and the digestibility of crude protein, ether extract, neutral detergent fiber, and acid detergent fiber (p < 0.05), but increases cecal acetate and butyrate concentrations, non-esterified fatty acids (NEFAs) in serum, and the ratio of dry matter intake to ADG(F/G). E1 diminished the activities of catalase and glutathione peroxidase, while it increased the content of interleukin, tumor necrosis factor-alpha, and reactive oxygen species (ROS) (p < 0.05). Cecal microbiome showed that the abundance of Firmicutes and Actinobacteria in E1 was significantly lower than in E2 (p = 0.029, p = 0.002), whereas Bacteroidetes was higher (p = 0.005). E1 increased the genera Ruminococcaceae-UCG-004, Acinetobacter, and Rikenellaceae_RC9_gut_group. Meanwhile, cecal metabolome showed that formyl-5-hydroxykynurenamine, chorismate, 3-sulfinoalanine, and 3-isopropylmalate were upregulated in E1, while brassinolide was downregulated. The altered metabolites were mainly enriched in metabolic pathways related to energy metabolism and metabolism to mitigate oxidative stress in the meat donkeys, such as tryptophan metabolism, brassinosteroid biosynthesis metabolism, etc. In conclusion, low-energy diets resulted in a negative energy balance in meat donkeys, resulting in more nutrients being oxidized to provide energy, inducing oxidative stress, and thereby leading to decreasing growth. The reduction in meat donkey growth from low-energy diets was related to changes in cecum microbiota and metabolites.

TMIC-15. GUT MICROBIOTA CONTROLS NEUROFIBROMATOSIS-1 (NF1) OPTIC GLIOMA GROWTH THROUGH IMMUNE CIRCUIT MODULATION

Abstract Changes in the gut microbiome can have profound effects on the nervous system through modulation of T cell and microglia function. Since our prior studies demonstrated that T cells and microglia positively regulate low-grade glioma growth through the establishment of T cell-microglia immune circuit, we sought to explore the impact of changes in the gut microbiota on tumor biology. For these studies, genetically engineered Neurofibromatosis type 1 (NF1) optic glioma (Nf1-OPG) mice were raised in a germ-free environment or treated with antibiotics to deplete gut bacteria. First, we demonstrated that Nf1-OPG mice raised in a germ-free (gnotobiotic) environment or treated with specific antibiotics lacked optic gliomas and had improved OPG-induced retinal pathology (increased retinal nerve fiber layer thickness). Second, germ-free and antibiotic-treated Nf1-OPG mice gavaged with fecal microbiota from Nf1-OPG mice raised in a standard barrier facility restored optic glioma growth. Third, we showed that both germ-free and antibiotic-treated Nf1-OPG mice exhibited reduced intra-tumoral CD8+ T cell content resulting from decreased microglia chemokine production. Fourth, we discovered a gut-brain paracrine axis whose interruption reduced optic glioma growth and attenuated retinal nerve fiber layer thinning. Collectively, these findings establish a mechanistic relationship between the gut microbiota and brain tumor growth relevant to potential therapeutic interventions for pediatric low-grade gliomas.

Clinical outcomes and associated bacterial and fungal microbiota changes after high dose probiotic therapy for severe alcohol-associated hepatitis: An observational study.

Alcohol-associated hepatitis (AH) is a critical condition with high mortality rates and is worsened by infections. Organ failure is strongly associated with intestinal dysbiosis. Emerging research suggests that gut microbiota modulation with probiotics can improve AH outcomes. This study investigated the clinical and microbiome effects of high-dose probiotic infusion (HDPI) compared with corticosteroid therapy (CST) and fecal microbiota transplantation (FMT) in severe AH. Patients with biopsy-proven severe-AH were enrolled from March 2019 to June 2020 and matched for age and disease severity. The patients received HDPI (n = 20), FMT (n = 16), or CST (n = 14). HDPI consists of a potent probiotic mix delivered via a nasoduodenal tube for 6 days. The primary outcome was survival at 90-days. Stool samples were subjected to 16S and 18S rRNA sequencing to assess significant bacterial and fungal taxa and their interactions at baseline and post treatment. At 90-days, survival rates were 55%, 64.3%, and 87.5% (HDPI, CST, respectively). HDPI did not beneficially impact bacterial alpha-diversity but significantly altered beta-diversity. Notably, the number of pathogenic bacteria, such as Bilophila and Roseburia increased. Fungal analysis revealed no significant changes in alpha diversity, but significant dissimilarities in beta diversity post-HDPI. New fungal genera such as Basidiomycota and Phragmoplastophyta have emerged, with significant deleterious expansion in fungal communities and damaging modifications between fungal-bacterial interactions. HDPI failed to outperform CST in improving the clinical outcomes of patients with severe AH. While HDPI influenced both bacterial and fungal microbiomes, it also led to the persistence of pathogenic communities. FMT showed superior survival outcomes, highlighting the urgent need for further controlled trials.

Unveiling the distinctive variations in multi-omics triggered by TP53 mutation in lung cancer subtypes: An insight from interaction among intratumoral microbiota, tumor microenvironment, and pathology

The TP53 mutation is one of the most common gene mutations in non-small cell lung cancer (NSCLC) and plays a significant role in the occurrence, development, and prognosis of both lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC). Recent studies have also suggested the predictive value of TP53 mutations in the response to immunotherapy for NSCLC. It is known that intratumoral microbiota, tumor immune microenvironment (TIME) and histology are associated with the roles of TP53 mutation in NSCLC. However, the intrinsic associations among these three factors and their underlying interaction with TP53 mutation are not well understood. Additionally, the potential of predicting TP53 mutations using deep learning methods has not yet been fully evaluated. In this paper, we comprehensively evaluated the tissue microbiome, host gene expression characteristics, and histopathological slides of 992 NSCLC patients obtained from the cancer genome atlas (TCGA) and validated the findings using multi-omics data of 332 NSCLC patients from the Clinical Proteomic Tumor Analysis Consortium (CPTAC). Compared to LUSC, LUAD exhibited more substantial differences between patients with and without TP53 mutation in all three aspects. In LUAD, our results imply underlying links between the tissue microbiome and immune cell components in the TIME, and show that the abundance of immune cells is reflected in histology slides. Furthermore, we propose a novel multimodal deep learning model that focuses on histopathology images, which achieves an area under the curve (AUC) of 0.84 in LUAD. In summary, TP53 mutation of LUAD resulted more significant changes in intratumoral microbiota, TIME and histology than that of LUSC. And histopathology images can be used to predict TP53 mutation in LUAD with reasonable accuracy.

Tetrandrine Alleviates Pulmonary Fibrosis by Modulating Lung Microbiota-Derived Metabolism and Ameliorating Alveolar Epithelial Cell Senescence.

Tetrandrine (TET) is a minimally toxic drug extracted from the root of Stephania tetrandra. We previously demonstrated that TET could ameliorate pulmonary fibrosis (PF) by modulating autophagy. However, the mechanism behind TET's protective effects on PF remains unclear. In this study, we utilized 16S rRNA gene sequencing, nontargeted metabolomic analysis, and network pharmacology to identify changes in lung microbiota and metabolites that mediate alveolar epithelial cell senescence in bleomycin (BLM)-induced PF in mice. Additionally, we employed Western blot analysis, RT-PCR, and immunofluorescence staining to investigate the invitro and invivo effects of TET and its influential bacterial metabolites on PF. The TET intervention alleviated PF by regulating the compositions of lung microbial communities (Streptococcus, Micrococcus, Acinetobacter, Altererythrobacter, Atopostipes, Candidatus Cloacimonas, Clostridium sensu stricto 1, Sphingomonas, Listeria, Blautia, and Pseudomonas) and metabolites (3,4-dihydroxyphenylpropionic acid (3,4-DHPPA), 6-Aminonicotinamide, N-acetyl-5-methoxykynuramine, and resiniferatoxin). Through network pharmacological analysis, it was determined that 3,4-DHPPA played a crucial role in alleviating PF by further inhibiting the senescence of alveolar epithelial cells, a finding further validated in exvivo experiments. TET mitigated BLM-induced PF in murine models through the modulation of lung microbiota composition and metabolism. Specifically, TET augmented the level of the microbiota-derived metabolite, 3,4-DHPPA, which in turn attenuated alveolar epithelial cell senescence.

Behavior, hormone, and gut microbiota change by YYNS intervention in an OVX mouse model

Behavior, hormone, and gut microbiota change by YYNS intervention in an OVX mouse model

Debate on the relationship between Helicobacter pylori infection and inflammatory bowel disease: a bibliometric analysis

BackgroundInflammatory bowel diseases (IBD) are chronic inflammation conditions affecting the gastrointestinal tract. Studies point out an association between Helicobacter pylori (H. pylori) infection and IBD. This study aims to visually assess the research trends and hotspots in the field of H. pylori infection and IBD, review mainstream perspectives in this field, and provide a foundation for future research and treatment.MethodsWe searched the Web of Science Core Collection Database for literature related to H. pylori and IBD, using VOS viewer to generate visual charts.ResultsA total of 246 publications were included, with articles being the predominant type of document. A significant increase in the number of publications was observed after 2011. China contributed the most of researches. Keyword clusters revealed that the researches primarily focused on immune mechanism, gut microbiome, diagnosis and treatment of IBD. Time trend results indicated that current researches centered on gut microbiota and immune mechanisms.ConclusionH. pylori infection may have a protective effect on IBD. The exact mechanisms remain unclear and may involve immunomodulation and changes of gut microbiota. Further researches are necessary for better understanding this relationship and its implications for clinical practice. Further researches and clinical practice should pay attention to this topic.

Endophytic Bacillus velezensis GsB01 controls Gleditsia sinensis wilt by secreting antifungal metabolites and modulates symbiotic microbiota within trees.

Identifying effective biological control agents against fungal pathogens and determining their mechanisms of action are important in the control of plant diseases. In this study, we isolated an endophytic bacterial strain, GsB01, from the branches of asymptomatic Gleditsia sinensis. Multi-locus sequence analysis identified the strain as Bacillus velezensis. GsB01 exhibited significant antifungal activity against Thyronectria austroamericana, the causative agent of G. sinensis wilt. Liquid chromatography-mass spectrometry identified four consistently present antimicrobial compounds in GsB01 metabolite fractions with high antifungal activity: macrolactin A, bacillaene A, surfactin, and iturin. GsB01's active metabolite fractions altered the metabolic profiles of T. austroamericana, disrupting seven pathways, including arginine biosynthesis, nucleotide metabolism, purine metabolism, and the pentose phosphate pathway. Furthermore, absolute quantitative polymerase chain reaction analysis suggested that GsB01 may increase the abundance of endophytic bacteria in G. sinensis. The 16S rRNA amplicon sequencing revealed changes in the endophytic landscape in stems and roots following GsB01 introduction, particularly with significant variation in the dominant bacterial genera within the stems. The study highlights GsB01's potential against plant wilt and suggests that its antifungal activity is achieved by secreting antifungal metabolites. The study also recorded changes in the symbiotic microbiota within trees that had been infected with a pathogenic fungus and subsequently treated with an endophytic antagonistic bacterial strain. © 2024 Society of Chemical Industry.

Mediterranean Diet and Olive Oil Redox Interactions on Lactate Dehydrogenase Mediated by Gut Oscillibacter in Patients with Long-COVID-19 Syndrome

Chronic viral inflammation is associated with oxidative stress and changes in gut microbiota. The Mediterranean diet (MD), with recognized anti-inflammatory and antioxidant properties, modulates gut microorganisms, specifically on the interaction between extra virgin olive oil, a key component of the MD with well-documented antioxidant effects. This study investigated the influence of adherence to MD and antioxidant-rich foods (extra virgin olive oil) on biochemical, inflammatory, and microbiota profiles in patients with chronic inflammation defined as a prolonged inflammatory response due to immune dysregulation following the acute phase of the viral infection. Participants were classified into low (n = 54) and high (n = 134) MD adherence groups (cut-off of 7 points based on previous studies utilizing the same threshold in the assessment of MD adherence). Gut microbiota was sequenced using the 16S technique, and the adherence to MD was assessed using a validated questionnaire for a Spanish population. High adherence to the MD was linked to significant improvements in inflammatory and oxidative stress markers, including reductions in LDL-cholesterol, glucose, and lactate dehydrogenase (LDH) levels, an indicative of redox balance, as well as a significant higher consumption of antioxidant foods. Moreover, gut microbiota analysis revealed distinct compositional shifts and a lower abundance of the Oscillibacter genus in the high adherence group. Notably, a significant interaction was observed between MD adherence and extra virgin olive oil consumption, with Oscillibacter abundance influencing LDH levels, suggesting that the MD antioxidant properties may modulate inflammation through gut microbiota-mediated mechanisms. These findings provide new evidence that adherence to the Mediterranean diet can reduce inflammatory markers in patients with long-COVID-19, a population that has not been extensively studied, while also highlighting the potential role of the bacterial genus Oscillibacter in modulating this effect.

Western diet promotes endometriotic lesion growth in mice and induces depletion of Akkermansia muciniphila in intestinal microbiota.

Endometriosis, affecting 10% of women in their reproductive years, remains poorly understood. Both individual and environmental unexplained factors are implicated in this heterogenous condition. This study aims to examine the influence of a Western diet on endometriosis lesion development in mice and to uncover the mechanisms involved. Mice were fed either a control diet or a Western diet (high in fatty acids and low in fiber) for 4weeks. Endometriosis was then surgically induced, and lesion development was monitored by ultrasound. After 7weeks, the mice were sacrificed for analysis of lesion characteristics through RT-qPCR, immunohistochemistry, and flow cytometry. Additionally, the intestinal microbiota was assessed using 16S rRNA gene sequencing. Mice on the Western diet developed lesions that were significantly twice as large compared to those on the control diet. These lesions exhibited greater fibrosis and proliferation, alongside enhanced macrophage activity and leptin pathway expression. Changes in the intestinal microbiota were significantly noted after endometriosis induction, regardless of diet. Notably, mice on the Western diet with the most substantial lesions showed a loss of Akkermansia Muciniphila in their intestinal microbiota. A Western diet significantly exacerbates lesion size in a mouse model of endometriosis, accompanied by metabolic and immune alterations. The onset of endometriosis also leads to substantial shifts in intestinal microbiota, suggesting a potential link between diet, intestinal health, and endometriosis development.