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Gut Mar 2020Pre-eclampsia (PE) is one of the malignant metabolic diseases that complicate pregnancy. Gut dysbiosis has been identified for causing metabolic diseases, but the role...
OBJECTIVE
Pre-eclampsia (PE) is one of the malignant metabolic diseases that complicate pregnancy. Gut dysbiosis has been identified for causing metabolic diseases, but the role of gut microbiome in the pathogenesis of PE remains unknown.
DESIGN
We performed a case-control study to compare the faecal microbiome of PE and normotensive pregnant women by 16S ribosomal RNA (rRNA) sequencing. To address the causative relationship between gut dysbiosis and PE, we used faecal microbiota transplantation (FMT) in an antibiotic-treated mouse model. Finally, we determined the microbiome translocation and immune responses in human and mouse placental samples by 16S rRNA sequencing, quantitative PCR and in situ hybridisation.
RESULTS
Patients with PE showed reduced bacterial diversity with obvious dysbiosis. Opportunistic pathogens, particularly and , were enriched, whereas beneficial bacteria, including and , were markedly depleted in the PE group. The abundances of these discriminative bacteria were correlated with blood pressure (BP), proteinuria, aminotransferase and creatinine levels. On successful colonisation, the gut microbiome from patients with PE triggered a dramatic, increased pregestational BP of recipient mice, which further increased after gestation. In addition, the PE-transplanted group showed increased proteinuria, embryonic resorption and lower fetal and placental weights. Their T regulatory/helper-17 balance in the small intestine and spleen was disturbed with more severe intestinal leakage. In the placenta of both patients with PE and PE-FMT mice, the total bacteria, , and inflammatory cytokine levels were significantly increased.
CONCLUSIONS
This study suggests that the gut microbiome of patients with PE is dysbiotic and contributes to disease pathogenesis.
Topics: Animals; Bacterial Translocation; Blood Pressure; CD4 Lymphocyte Count; Case-Control Studies; Chemokines; Creatinine; Cytokines; Disease Models, Animal; Dysbiosis; Faecalibacterium; Feces; Female; Fetal Resorption; Fusobacteria; Gastrointestinal Microbiome; Humans; Intestine, Small; Mice; Placenta; Pre-Eclampsia; Pregnancy; Proteinuria; RNA, Messenger; T-Lymphocytes, Regulatory; Th17 Cells; Veillonella
PubMed: 31900289
DOI: 10.1136/gutjnl-2019-319101 -
The Journal of Infection Jul 2020Breastfeeding is associated with considerable health benefits for infants. Aside from essential nutrients, immune cells and bioactive components, breast milk also... (Review)
Review
Breastfeeding is associated with considerable health benefits for infants. Aside from essential nutrients, immune cells and bioactive components, breast milk also contains a diverse range of microbes, which are important for maintaining mammary and infant health. In this review, we summarise studies that have investigated the composition of the breast milk microbiota and factors that might influence it. We identified 44 studies investigating 3105 breast milk samples from 2655 women. Several studies reported that the bacterial diversity is higher in breast milk than infant or maternal faeces. The maximum number of each bacterial taxonomic level detected per study was 58 phyla, 133 classes, 263 orders, 596 families, 590 genera, 1300 species and 3563 operational taxonomic units. Furthermore, fungal, archaeal, eukaryotic and viral DNA was also detected. The most frequently found genera were Staphylococcus, Streptococcus Lactobacillus, Pseudomonas, Bifidobacterium, Corynebacterium, Enterococcus, Acinetobacter, Rothia, Cutibacterium, Veillonella and Bacteroides. There was some evidence that gestational age, delivery mode, biological sex, parity, intrapartum antibiotics, lactation stage, diet, BMI, composition of breast milk, HIV infection, geographic location and collection/feeding method influence the composition of the breast milk microbiota. However, many studies were small and findings sometimes contradictory. Manipulating the microbiota by adding probiotics to breast milk or artificial milk offers an exciting avenue for future interventions to improve infant health.
Topics: Animals; Breast Feeding; Female; HIV Infections; Humans; Infant; Lactation; Microbiota; Milk, Human; Pregnancy
PubMed: 32035939
DOI: 10.1016/j.jinf.2020.01.023 -
Clinics in Liver Disease Feb 2024Genome-wide association analyses suggest that HLA genes including HLA-DRB*0301, HLA-DRB*0401, and HLA-B*3501 as well as non-HLA genes including CD28/CTLA4/ICOS and SYNPR... (Review)
Review
Genome-wide association analyses suggest that HLA genes including HLA-DRB*0301, HLA-DRB*0401, and HLA-B*3501 as well as non-HLA genes including CD28/CTLA4/ICOS and SYNPR increased AIH susceptibility. The destruction of hepatocytes is the result of the imbalance between proinflammatory cells and immunosuppressive cells, especially the imbalance between Tregs and Th17 cells. The microbiome in patients with AIH is decreased in diversity with a specific decline in Bifidobacterium and enrichment in Veillonella and Faecalibacterium. Recent evidence has demonstrated the pathogenic role of E. gallinarum and L.reuteri in inducing autoimmunity in the liver.
Topics: Humans; Hepatitis, Autoimmune; Genome-Wide Association Study; Autoimmunity; Immunosuppressive Agents
PubMed: 37945156
DOI: 10.1016/j.cld.2023.06.003 -
Frontiers in Cellular and Infection... 2021Graves' disease (GD) is a clinical syndrome with an enlarged and overactive thyroid gland, an accelerated heart rate, Graves' orbitopathy (GO), and pretibial myxedema... (Review)
Review
Graves' disease (GD) is a clinical syndrome with an enlarged and overactive thyroid gland, an accelerated heart rate, Graves' orbitopathy (GO), and pretibial myxedema (PTM). GO is the most common extrathyroidal complication of GD. GD/GO has a significant negative impact on the quality of life. GD is the most common systemic autoimmune disorder, mediated by autoantibodies to the thyroid-stimulating hormone receptor (TSHR). It is generally accepted that GD/GO results from complex interactions between genetic and environmental factors that lead to the loss of immune tolerance to thyroid antigens. However, the exact mechanism is still elusive. Systematic investigations into GD/GO animal models and clinical patients have provided important new insight into these disorders during the past 4 years. These studies suggested that gut microbiota may play an essential role in the pathogenesis of GD/GO. Antibiotic vancomycin can reduce disease severity, but fecal material transfer (FMT) from GD/GO patients exaggerates the disease in GD/GO mouse models. There are significant differences in microbiota composition between GD/GO patients and healthy controls. , , and often increase in GD patients. The commonly used therapeutic agents for GD/GO can also affect the gut microbiota. Antigenic mimicry and the imbalance of T helper 17 cells (Th17)/regulatory T cells (Tregs) are the primary mechanisms proposed for dysbiosis in GD/GO. Interventions including antibiotics, probiotics, and diet modification that modulate the gut microbiota have been actively investigated in preclinical models and, to some extent, in clinical settings, such as probiotics () and selenium supplements. Future studies will reveal molecular pathways linking gut and thyroid functions and how they impact orbital autoimmunity. Microbiota-targeting therapeutics will likely be an essential strategy in managing GD/GO in the coming years.
Topics: Animals; Gastrointestinal Microbiome; Graves Disease; Graves Ophthalmopathy; Humans; Mice; Quality of Life; Receptors, Thyrotropin
PubMed: 35004341
DOI: 10.3389/fcimb.2021.739707 -
Journal of Cachexia, Sarcopenia and... Dec 2021Cancer cachexia is characterized by a negative energy balance, muscle and adipose tissue wasting, insulin resistance, and systemic inflammation. Because of its strong...
BACKGROUND
Cancer cachexia is characterized by a negative energy balance, muscle and adipose tissue wasting, insulin resistance, and systemic inflammation. Because of its strong negative impact on prognosis and its multifactorial nature that is still not fully understood, cachexia remains an important challenge in the field of cancer treatment. Recent animal studies indicate that the gut microbiota is involved in the pathogenesis and manifestation of cancer cachexia, but human data are lacking. The present study investigates gut microbiota composition, short-chain fatty acids (SCFA), and inflammatory parameters in human cancer cachexia.
METHODS
Faecal samples were prospectively collected in patients (N = 107) with pancreatic cancer, lung cancer, breast cancer, or ovarian cancer. Household partners (N = 76) of the patients were included as healthy controls with similar diet and environmental conditions. Patients were classified as cachectic if they lost >5% body weight in the last 6 months. Gut microbiota composition was analysed by sequencing of the 16S rRNA V4 gene region. Faecal SCFA levels were quantified by gas chromatography. Faecal calprotectin was assessed with enzyme-linked immunosorbent assay. Serum C-reactive protein and leucocyte counts were retrieved from medical records.
RESULTS
Cachexia prevalence was highest in pancreatic cancer (66.7%), followed by ovarian cancer (25%), lung cancer (20.8%), and breast cancer (17.3%). Microbial α-diversity was not significantly different between cachectic cancer patients (N = 33), non-cachectic cancer patients (N = 74), or healthy controls (N = 76) (species richness P = 0.31; Shannon effective index P = 0.46). Community structure (β-diversity) tended to differ between these groups (P = 0.053), although overall differences were subtle and no clear clustering of samples was observed. Proteobacteria (P < 0.001), an unknown genus from the Enterobacteriaceae family (P < 0.01), and Veillonella (P < 0.001) were more abundant among cachectic cancer patients. Megamonas (P < 0.05) and Peptococcus (P < 0.001) also showed differential abundance. Faecal levels of all SCFA tended to be lower in cachectic cancer patients, but only acetate concentrations were significantly reduced (P < 0.05). Faecal calprotectin levels were positively correlated with the abundance of Peptococcus, unknown Enterobacteriaceae, and Veillonella. We also identified several correlations and interactions between clinical and microbial parameters.
CONCLUSIONS
This clinical study provided the first insights into the alterations of gut microbiota composition and SCFA levels that occur in cachectic cancer patients and how they are related to inflammatory parameters. These results pave the way for further research examining the role of the gut microbiota in cancer cachexia and its potential use as therapeutic target.
Topics: Animals; Cachexia; Fatty Acids, Volatile; Gastrointestinal Microbiome; Humans; Pancreatic Neoplasms; RNA, Ribosomal, 16S
PubMed: 34609073
DOI: 10.1002/jcsm.12804 -
Journal of Advanced Research Jan 2023Considerable evidence has linked periodontitis (PD) to hypertension (HTN), but the nature behind this connection is unclear. Dysbiosis of oral microbiota leading to PD...
INTRODUCTION
Considerable evidence has linked periodontitis (PD) to hypertension (HTN), but the nature behind this connection is unclear. Dysbiosis of oral microbiota leading to PD is known to aggravate different systematic diseases, but the alteration of oral microbiota in HTN and their impacts on blood pressure (BP) remains to be discovered.
OBJECTIVES
To characterize the alterations of oral and gut microbiota and their roles in HTN.
METHODS
We performed a cross-sectional (95 HTN participants and 39 controls) and a 6-month follow-up study (52 HTN participants and 26 controls) to analyze the roles of oral and gut microbiota in HTN. Saliva, subgingival plaques, and feces were collected for 16S rRNA gene sequencing or metagenomic analysis. C57BL/6J mice were pretreated with antibiotics to deplete gut microbiota, and then transplanted with human saliva by gavage to test the impacts of abnormal oral-gut microbial transmission on HTN.
RESULTS
BP in participants with PD was higher than no PD in both cross-sectional and follow-up cohort. Relative abundances of 14 salivary genera, 15 subgingival genera and 10 gut genera significantly altered in HTN and those of 7 salivary genera, 12 subgingival genera and 6 gut genera significantly correlated with BP. Sixteen species under 5 genera were identified as oral-gut transmitters, illustrating the presence of oral-gut microbial transmission in HTN. Veillonella was a frequent oral-gut transmitter stably enriched in HTN participants of both cross-sectional and follow-up cohorts. Saliva from HTN participants increased BP in hypertensive mice. Human saliva-derived Veillonella successfully colonized in mouse gut, more abundantly under HTN condition.
CONCLUSIONS
PD and oral microbiota are strongly associated with HTN, likely through oral-gut transmission of microbes. Ectopic colonization of saliva-derived Veillonella in the gut may aggravate HTN. Therefore, precise manipulations of oral microbiota and/or oral-gut microbial transmission may be useful strategies for better prevention and treatment of HTN.
Topics: Humans; Animals; Mice; Gastrointestinal Microbiome; RNA, Ribosomal, 16S; Cross-Sectional Studies; Follow-Up Studies; Mice, Inbred C57BL; Microbiota; Hypertension; Periodontitis
PubMed: 36585105
DOI: 10.1016/j.jare.2022.03.007 -
Frontiers in Cellular and Infection... 2021Regulating the composition of human breastmilk has the potential to prevent allergic diseases early in life. The composition of breastmilk is complex, comprising varying...
Regulating the composition of human breastmilk has the potential to prevent allergic diseases early in life. The composition of breastmilk is complex, comprising varying levels of oligosaccharides, immunoactive molecules, vitamins, metabolites, and microbes. Although several studies have examined the relationship between different components of breastmilk and infant food allergies, few have investigated the relationship between microorganisms in breastmilk and infant food allergy. In the present study, we selected 135 healthy pregnant women and their full-term newborns from a cohort of 202 mother-infant pairs. Among them, 69 infants were exclusively breastfed until 6 mo after birth. At follow-up, 11 of the 69 infants developed a food allergy in infancy while 22 showed no signs of allergy. Thirty-three breastmilk samples were collected within 1 mo after delivery, and 123 infant fecal samples were collected at five time points following their birth. These samples were analyzed using microbial 16S rRNA gene sequencing. The abundance and evenness of the milk microbiota and the number of differential bacteria were higher in the breastmilk samples from the non-allergy group than in those from the food allergy group. The non-allergy group showed relatively high abundance of , , IV, XIVa, , and butyrate-producing bacteria such as , , , and . In contrast, the abundance of , , and in breastmilk was higher in the food allergy group. A comparison of the changes in dominant differential breastmilk microbiota in the intestinal flora of the two groups of infants over time revealed that the changes in abundance were consistent with those in the breastmilk flora. Functional pathway prediction of breastmilk microflora showed that the enhancement of the metabolic pathways of tyrosine, tryptophan, and fatty acids was significantly different between the groups. We suggest that changes in the breastmilk microbiota can influence the development of food allergies. Breastmilk contains several microbes that have protective effects against food allergies, both by influencing the colonization of intestinal microbiota and by producing butyrate. This study may provide new ideas for improving infant health through early intervention with probiotics.
Topics: Feces; Female; Food Hypersensitivity; Gastrointestinal Microbiome; Humans; Infant; Infant, Newborn; Microbiota; Milk, Human; Pregnancy; RNA, Ribosomal, 16S
PubMed: 35096637
DOI: 10.3389/fcimb.2021.770913 -
Frontiers in Psychiatry 2020Cumulative evidence shows a linkage between gut microbiota pattern and depression through the brain-gut microbiome axis. The aim of this systematic review was to...
Cumulative evidence shows a linkage between gut microbiota pattern and depression through the brain-gut microbiome axis. The aim of this systematic review was to identify the alterations of the gut microbiota patterns in people with depression compared to healthy controls. A comprehensive literature search of human studies, published between January 2000 and June 2019, was reviewed. The key words included gastrointestinal microbiome, gut microbiome, microbiota, depression, depressive symptoms, and depressive disorder. The systematic review adhered to the Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) guidelines. Nine articles met the eligibility criteria. Disparities in α-diversity and β-diversity of the microbiota existed in people with depression compared to healthy controls. At the phylum level, there were inconsistencies in the abundance of , , . However, high abundance in and phyla were observed in people with depression. On the family level, high abundance of , , , , , , , , , , , , , low abundance of , , , , , , and were observed in people with depression. On the genus level, high abundance of , , , , , , , , , , , , , , , , , , , , , , , and low abundance of , , , , , , , and were found in people with depression. Alteration of gut microbiome patterns was evident in people with depression. Further evidence is warranted to allow for the translation of microbiome findings toward innovative clinical strategies that may improve treatment outcomes in people with depression.
PubMed: 32587537
DOI: 10.3389/fpsyt.2020.00541 -
Archives of Microbiology Jul 2022The influence of microbiota on the human body is currently the subject of many studies. The composition of bacteria colonizing the gastrointestinal tract varies... (Review)
Review
The influence of microbiota on the human body is currently the subject of many studies. The composition of bacteria colonizing the gastrointestinal tract varies depending on genetic make-up, lifestyle, use of antibiotics or the presence of diseases. The diet is also important in the species diversity of the microbiota. This study is an analysis of the relationships between physical activity, diet, and the microbiota of the gastrointestinal tract in athletes. This review shows the differences in the microbial composition in various sports disciplines, the influence of probiotics on the microbiome, the consequence of which may be achieved even better sports results. Physical activity increases the number of bacteria, mainly of the Clostridiales order and the genus: Lactobacillus, Prevotella, Bacteroides, and Veillonella, and their number varies depending on the sports discipline. These bacteria are present in athletes in sports that require a high VO max. The players' diet also influences the composition of the microbiota. A diet rich in dietary fiber increases the amount of Lactobacillus or Bifidobacterium bacteria, probiotic microorganisms, which indicates the need to supplement the diet with probiotic preparations. It is impossible to suggest an unambiguous answer to how the microbiota of the gastrointestinal tract changes in athletes and requires further analyzes.
Topics: Bacteria; Bifidobacterium; Feces; Gastrointestinal Microbiome; Humans; Lactobacillus; Microbiota; Probiotics
PubMed: 35834007
DOI: 10.1007/s00203-022-03111-5 -
Nature Microbiology Oct 2022Colonization of the intestine by oral microbes has been linked to multiple diseases such as inflammatory bowel disease and colon cancer, yet mechanisms allowing...
Colonization of the intestine by oral microbes has been linked to multiple diseases such as inflammatory bowel disease and colon cancer, yet mechanisms allowing expansion in this niche remain largely unknown. Veillonella parvula, an asaccharolytic, anaerobic, oral microbe that derives energy from organic acids, increases in abundance in the intestine of patients with inflammatory bowel disease. Here we show that nitrate, a signature metabolite of inflammation, allows V. parvula to transition from fermentation to anaerobic respiration. Nitrate respiration, through the narGHJI operon, boosted Veillonella growth on organic acids and also modulated its metabolic repertoire, allowing it to use amino acids and peptides as carbon sources. This metabolic shift was accompanied by changes in carbon metabolism and ATP production pathways. Nitrate respiration was fundamental for ectopic colonization in a mouse model of colitis, because a V. parvula narG deletion mutant colonized significantly less than a wild-type strain during inflammation. These results suggest that V. parvula harness conditions present during inflammation to colonize in the intestine.
Topics: Adenosine Triphosphate; Amino Acids; Animals; Carbon; Inflammation; Inflammatory Bowel Diseases; Intestines; Mice; Nitrates; Veillonella
PubMed: 36138166
DOI: 10.1038/s41564-022-01224-7