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1.
Nat Commun ; 10(1): 2012, 2019 05 01.
Artigo em Inglês | MEDLINE | ID: mdl-31043597

RESUMO

Small intestinal bacterial overgrowth (SIBO) has been implicated in symptoms associated with functional gastrointestinal disorders (FGIDs), though mechanisms remain poorly defined and treatment involves non-specific antibiotics. Here we show that SIBO based on duodenal aspirate culture reflects an overgrowth of anaerobes, does not correspond with patient symptoms, and may be a result of dietary preferences. Small intestinal microbial composition, on the other hand, is significantly altered in symptomatic patients and does not correspond with aspirate culture results. In a pilot interventional study we found that switching from a high fiber diet to a low fiber, high simple sugar diet triggered FGID-related symptoms and decreased small intestinal microbial diversity while increasing small intestinal permeability. Our findings demonstrate that characterizing small intestinal microbiomes in patients with gastrointestinal symptoms may allow a more targeted antibacterial or a diet-based approach to treatment.


Assuntos
Disbiose/microbiologia , Gastroenteropatias/microbiologia , Microbioma Gastrointestinal/fisiologia , Mucosa Intestinal/metabolismo , Intestino Delgado/microbiologia , Adolescente , Adulto , Idoso , Idoso de 80 Anos ou mais , Antibacterianos , DNA Bacteriano/isolamento & purificação , Fibras na Dieta/administração & dosagem , Açúcares da Dieta/efeitos adversos , Disbiose/dietoterapia , Disbiose/tratamento farmacológico , Disbiose/fisiopatologia , Feminino , Gastroenteropatias/dietoterapia , Gastroenteropatias/tratamento farmacológico , Gastroenteropatias/fisiopatologia , Voluntários Saudáveis , Humanos , Mucosa Intestinal/microbiologia , Mucosa Intestinal/fisiopatologia , Intestino Delgado/metabolismo , Intestino Delgado/fisiopatologia , Masculino , Pessoa de Meia-Idade , Permeabilidade , Projetos Piloto , Adulto Jovem
2.
Crit Rev Oncol Hematol ; 139: 31-40, 2019 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-31112880

RESUMO

Imbalance within the resident bacterial community (dysbiosis), rather than the presence and activity of a single organism, has been proposed to be associated with, and to influence, the development and progression of various diseases; however, the existence and significance of dysbiosis in oral/oropharyngeal cancer is yet to be clearly established. A systematic search (conducted on 25/01/2018 and updated on 25/05/2018) was performed on three databases (Pubmed, Web of Science & Scopus) to identify studies employing culture-independent methods which investigated the bacterial community in oral/oropharyngeal cancer patients compared to control subjects. Of the 1546 texts screened, only fifteen publications met the pre-determined selection criteria. Data extracted from 731 cases and 809 controls overall, could not identify consistent enrichment of any particular taxon in oral/oropharyngeal cancers, although common taxa could be identified between studies. Six studies reported the enrichment of Fusobacteria in cancer at different taxonomic levels whereas four studies reported an increase in Parvimonas. Changes in microbial diversity remained inconclusive, with four studies showing a higher diversity in controls, three studies showing a higher diversity in tumors and three additional studies showing no difference between tumors and controls. Even though most studies identified a component of dysbiosis in oral/oropharyngeal cancer, methodological and analytical variations prevented a standardized summary, which highlights the necessity for studies of superior quality and magnitude employing standardized methodology and reporting. Indeed an holistic metagenomic approach is likely to be more meaningful, as is understanding of the overall metabolome, rather than a mere enumeration of the organisms present.


Assuntos
Carcinoma de Células Escamosas/epidemiologia , Disbiose/complicações , Neoplasias Bucais/epidemiologia , Neoplasias Orofaríngeas/epidemiologia , Carcinoma de Células Escamosas/microbiologia , Bases de Dados Factuais , Disbiose/fisiopatologia , Humanos , Incidência , Metanálise como Assunto , Neoplasias Bucais/microbiologia , Neoplasias Orofaríngeas/microbiologia
4.
Invest Ophthalmol Vis Sci ; 60(5): 1384-1393, 2019 04 01.
Artigo em Inglês | MEDLINE | ID: mdl-30938773

RESUMO

Purpose: In this study, the gut fungal microbiome of uveitis (UVT) patients was generated and compared with healthy controls (HC) to identify dysbiosis in UVT patients and ascertain the role of gut fungal microbiome in disease pathology. Methods: In the present study, gut fungal microbiomes were analyzed in the fecal samples of HC (n = 24) and UVT patients (n = 14) using high-throughput Illumina sequencing of ITS2 region of the fungal ribosomal RNA. QIIME and R software were used for data analysis. Results: The gut fungal richness and diversity were significantly decreased in UVT patients compared to HC. Our analyses showed enrichment of several pathogenic fungi including Malassezia restricta, Candida albicans, Candida glabrata, and Aspergillus gracilis in UVT patients. Heatmap and discriminatory OTUs further confirmed the disparities between UVT and HC microbiomes. Conclusions: This is the first study demonstrating dysbiosis in the gut fungal communities of UVT patients indicating the importance of fungal microbiome in the disease pathology. These initial findings might warrant further investigation into the fungal microbiome, especially interactions between fungal and bacterial that then might give further insight into how probiotics or fecal transplants might benefit.


Assuntos
Disbiose/fisiopatologia , Microbioma Gastrointestinal/fisiologia , Uveíte/microbiologia , Adulto , Idoso , Idoso de 80 Anos ou mais , Bactérias/genética , Estudos de Casos e Controles , Fezes/microbiologia , Feminino , Fungos , Humanos , Masculino , Pessoa de Meia-Idade , RNA Ribossômico 16S/genética , Adulto Jovem
5.
World J Gastroenterol ; 25(5): 552-566, 2019 Feb 07.
Artigo em Inglês | MEDLINE | ID: mdl-30774271

RESUMO

Despite their high prevalence, lack of understanding of the exact pathophysiology of the functional gastrointestinal disorders has restricted us to symptomatic diagnostic tools and therapies. Complex mechanisms underlying the disturbances in the bidirectional communication between the gastrointestinal tract and the brain have a vital role in the pathogenesis and are key to our understanding of the disease phenomenon. Although we have come a long way in our understanding of these complex disorders with the help of studies on animals especially rodents, there need to be more studies in humans, especially to identify the therapeutic targets. This review study looks at the anatomical features of the gut-brain axis in order to discuss the different factors and underlying molecular mechanisms that may have a role in the pathogenesis of functional gastrointestinal disorders. These molecules and their receptors can be targeted in future for further studies and possible therapeutic interventions. The article also discusses the potential role of artificial intelligence and machine learning and its possible role in our understanding of these scientifically challenging disorders.


Assuntos
Disbiose/fisiopatologia , Gastroenteropatias/fisiopatologia , Microbioma Gastrointestinal/fisiologia , Trato Gastrointestinal/inervação , Sistema Hipotálamo-Hipofisário/fisiopatologia , Animais , Antibacterianos/uso terapêutico , Diagnóstico por Computador/métodos , Disbiose/imunologia , Disbiose/microbiologia , Disbiose/terapia , Gastroenteropatias/diagnóstico , Gastroenteropatias/imunologia , Gastroenteropatias/terapia , Trato Gastrointestinal/imunologia , Trato Gastrointestinal/patologia , Trato Gastrointestinal/fisiopatologia , Humanos , Sistema Hipotálamo-Hipofisário/diagnóstico por imagem , Aprendizado de Máquina , Vias Neurais/fisiopatologia , Neuroimagem/métodos , Probióticos/administração & dosagem , Nervo Vago/fisiopatologia
6.
Trends Neurosci ; 42(3): 151-163, 2019 03.
Artigo em Inglês | MEDLINE | ID: mdl-30795845

RESUMO

From an evolutionary perspective, the genes of enteric microbes transmitted reliably across generations are nearly as much a part of the human organism as our own genes. Disruption of the microbiome leading to extinction of key 'heirloom' taxa can deprive individuals of metabolic pathways that have been present in their ancestors for millennia. Some of these pathways support essential synthesis and toxin clearance processes, including the generation of blood-brain barrier-crossing metabolic products crucial for normal brain function. Here, we discuss three such pathways: endogenous benzodiazepine synthesis, production of queuine/queuosine, and excretion of dietary mercury. Among them, these pathways have the potential to impact systems relevant to a wide range of neurodevelopmental and psychiatric conditions including autism, depression, anxiety, and schizophrenia.


Assuntos
Encéfalo/fisiopatologia , Depressão/fisiopatologia , Disbiose/fisiopatologia , Microbiota/fisiologia , Animais , Ansiedade/fisiopatologia , Humanos , Esquizofrenia/fisiopatologia
7.
Int J Mol Sci ; 20(4)2019 Feb 14.
Artigo em Inglês | MEDLINE | ID: mdl-30769793

RESUMO

Living organisms display internal biological rhythms, which are an evolutionarily conserved adaptation to the environment that drives their rhythmic behavioral and physiological activities. The gut microbiota has been proposed, in association with diet, to regulate the intestinal peripheral clock. However, the effect of gut dysbiosis on liver remains elusive, despite that germfree mice show alterations in liver metabolic functions and the hepatic daily rhythm. We analyzed whether the disruption of gut microbial populations with various antibiotics would differentially impact liver functions in mice. Our results support the notion of an impact on the hepatic biological rhythm by gram-positive bacteria. In addition, we provide evidence for differential roles of gut microbiota spectra in xenobiotic metabolism that could protect against the harmful pharmacological effects of drugs. Our results underscore a possible link between liver cell proliferation and gram-positive bacteria.


Assuntos
Relógios Circadianos/genética , Disbiose/genética , Microbioma Gastrointestinal/genética , Fígado/fisiologia , Animais , Proliferação de Células/efeitos dos fármacos , Disbiose/tratamento farmacológico , Disbiose/fisiopatologia , Microbioma Gastrointestinal/fisiologia , Bactérias Gram-Positivas/genética , Bactérias Gram-Positivas/fisiologia , Humanos , Intestinos/microbiologia , Intestinos/fisiologia , Fígado/efeitos dos fármacos , Fígado/microbiologia , Camundongos
8.
Infect Immun ; 87(5)2019 03.
Artigo em Inglês | MEDLINE | ID: mdl-30782858

RESUMO

Chitin is a natural N-acetylglucosamine polymer and a major structural component of fungal cell walls. Dietary chitin is mucoadhesive; anti-inflammatory effects of chitin microparticles (CMPs; 1- to 10-µm diameters) have been demonstrated in models of inflammatory bowel disease (IBD). The goals of this study were to assess (i) whether CMPs among various chitin preparations are the most effective against colitis in male and female mice and (ii) whether host chitin-binding Toll-like receptor 2 (TLR2) and CD14 are required for the anti-inflammatory effect of chitin. We found that colitis in male mice was ameliorated by CMPs and large chitin beads (LCBs; 40 to 70 µm) but not by chitosan (deacetylated chitin) microparticles, oligosaccharide chitin, or glucosamine. In fact, LCBs were more effective than CMPs. In female colitis, on the other hand, CMPs and LCBs were equally and highly effective. Neither sex of TLR2-deficient mice showed anti-inflammatory effects when treated with LCBs. No anti-inflammatory effect of LCBs was seen in either CD14-deficient males or females. Furthermore, an in vitro study indicated that when LCBs and CMPs were digested with stomach acidic mammalian chitinase (AMC), their size-dependent macrophage activations were modified, at least in part, suggesting reduced particle sizes of dietary chitin in the stomach. Interestingly, stomach AMC activity was greater in males than females. Our results indicated that dietary LCBs were the most effective preparation for treating colitis in both sexes; these anti-inflammatory effects of LCBs were dependent on host TLR2 and CD14.


Assuntos
Candida albicans/química , Quitina/uso terapêutico , Colite/dietoterapia , Colite/fisiopatologia , Disbiose/fisiopatologia , Ativação de Macrófagos/efeitos dos fármacos , Receptor 2 Toll-Like/efeitos dos fármacos , Animais , Modelos Animais de Doenças , Feminino , Humanos , Masculino , Camundongos , Camundongos Endogâmicos C57BL
9.
J Biomed Sci ; 26(1): 1, 2019 Jan 03.
Artigo em Inglês | MEDLINE | ID: mdl-30602371

RESUMO

Gut microbiota interacting with an intact mucosal surface are key to the maintenance of homeostasis and health. This review discusses the current state of knowledge of the biofilm mode of growth of these microbiota communities, and how in turn their disruptions may cause disease. Beyond alterations of relative microbial abundance and diversity, the aim of the review is to focus on the disruptions of the microbiota biofilm structure and function, the dispersion of commensal bacteria, and the mechanisms whereby these dispersed commensals may become pathobionts. Recent findings have linked iron acquisition to the expression of virulence factors in gut commensals that have become pathobionts. Causal studies are emerging, and mechanisms common to enteropathogen-induced disruptions, as well as those reported for Inflammatory Bowel Disease and colo-rectal cancer are used as examples to illustrate the great translational potential of such research. These new observations shed new light on our attempts to develop new therapies that are able to protect and restore gut microbiota homeostasis in the many disease conditions that have been linked to microbiota dysbiosis.


Assuntos
Fenômenos Fisiológicos Bacterianos , Biofilmes , Disbiose/fisiopatologia , Microbioma Gastrointestinal/fisiologia , Doenças Inflamatórias Intestinais/imunologia , Ferro/metabolismo , Disbiose/imunologia , Disbiose/microbiologia , Homeostase , Humanos , Doenças Inflamatórias Intestinais/complicações , Doenças Inflamatórias Intestinais/microbiologia , Simbiose
10.
Sci Total Environ ; 662: 246-253, 2019 Apr 20.
Artigo em Inglês | MEDLINE | ID: mdl-30690359

RESUMO

Microplastics (MPs) can be ingested by a variety of species and mainly accumulate in the gut. However, the consequences of MPs exposure in the gut are largely unknown. Here we evaluated the impacts of MPs exposure in zebrafish gut. Animals were experimentally exposed to polystyrene MPs (5-µm beads; 50 µg/L and 500 µg/L) for 21 days and monitored for alterations in tissue histology, enzymatic biomarkers, gut microbiome and metabolomic responses. Inflammation and oxidative stress were observed in the zebrafish gut after exposed to MPs. Furthermore, significant alterations in the gut microbiome and tissue metabolic profiles were observed, with most of these were associated with oxidative stress, inflammation and lipid metabolism. This study provides evidence that MPs exposure causes gut damage as well as alterations in gut metabolome and microbiome, yielding novel insights into the consequences of MPs exposure.


Assuntos
Disbiose/fisiopatologia , Doenças dos Peixes/imunologia , Inflamação/imunologia , Poliestirenos/efeitos adversos , Poluentes Químicos da Água/efeitos adversos , Peixe-Zebra , Animais , Relação Dose-Resposta a Droga , Disbiose/induzido quimicamente , Disbiose/imunologia , Doenças dos Peixes/induzido quimicamente , Doenças dos Peixes/fisiopatologia , Microbioma Gastrointestinal/efeitos dos fármacos , Inflamação/induzido quimicamente , Intestinos/imunologia , Intestinos/fisiologia , Metaboloma/efeitos dos fármacos , Metagenômica , Estresse Oxidativo/efeitos dos fármacos , Poliestirenos/metabolismo , Distribuição Aleatória , Testes de Toxicidade Crônica , Poluentes Químicos da Água/metabolismo , Peixe-Zebra/metabolismo , Peixe-Zebra/microbiologia
11.
Adv Exp Med Biol ; 1125: 25-36, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-30680646

RESUMO

Bacterial colonization patterns in preterm infants differ from those of their term counterparts due to maternal microbial diversity, delivery mode, feeding methods, antibiotic use, and exposure to commensal microbiota and pathogens in the neonatal intensive care unit (NICU). Early gut microbiome dysbiosis predisposes neonates to necrotizing enterocolitis (NEC), a devastating intestinal disease with high morbidity and mortality. Though mechanisms of NEC pathogenesis are not fully understood, the microbiome is a promising therapy target for prevention and treatment. Direct administration of probiotics to preterm infants has been shown to reduce the incidence of NEC, but is not without risk. The immature immune systems of preterm infants leave them vulnerable to even beneficial bacteria. Further research is required to investigate both short-term and long-term effects of probiotic administration to preterm infants. Other methods of altering the preterm infant microbiome must also be considered, including breastfeeding, prebiotics, and targeting the maternal microbiome.


Assuntos
Disbiose/fisiopatologia , Enterocolite Necrosante/microbiologia , Microbioma Gastrointestinal , Doenças do Prematuro/microbiologia , Recém-Nascido Prematuro , Probióticos/uso terapêutico , Humanos , Recém-Nascido
12.
J Gynecol Obstet Hum Reprod ; 48(4): 223-229, 2019 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-30685426

RESUMO

An abnormal vaginal microbiota composition has been shown to lead to pre-term births, miscarriage, and problems with conceiving. Studies have suggested that dysbiosis reduces successful early pregnancy development during IVF. However, conflicting reports exist. This meta-analysis aims to answer the following question: what is the aggregated effect found by studies investigating the influence of the vaginal microbiota composition on early pregnancy rates after IVF treatment? A systematic review was performed using the Medline and EMBASE databases, using search terms for healthy vaginal microbiota, abnormal vaginal microbiota, fertility and pregnancy. The search resulted in six included articles. Of these, all six were used for further meta-analysis. The main outcome measures were the clinical pregnancy rate, determined through ultrasound proven fetal heartbeat and/or hCG results before 10 weeks gestation, in relation to the vaginal microbiota composition. We found a correlation between abnormal vaginal microbiota and lower rates of early pregnancy development after IVF treatment (OR = 0.70, 95% CI = 0.49 - 0.99). One study showed the reverse correlation. However, heterogeneity between study methodologies in various forms was found. In conclusion, women with an abnormal vaginal microbiota are roughly 1.4 times less likely to have a successful early pregnancy development after IVF treatment when compared to women with normal microbiota.


Assuntos
Fertilização In Vitro , Microbiota/fisiologia , Vagina/microbiologia , Disbiose/complicações , Disbiose/fisiopatologia , Transferência Embrionária , Feminino , Fertilidade/fisiologia , Humanos , MEDLINE , Gravidez , Resultado da Gravidez , Taxa de Gravidez , Staphylococcus aureus/isolamento & purificação , Resultado do Tratamento , Estreptococos Viridans/isolamento & purificação
13.
Acta Biochim Biophys Sin (Shanghai) ; 51(1): 88-96, 2019 Jan 01.
Artigo em Inglês | MEDLINE | ID: mdl-30544157

RESUMO

Propamocarb (PM) is a pesticide that is widely used to protect cucumbers and other plants from downy mildew. Recently, some studies indicated that PM exposure had potential toxic effects in animals. In this study, adult male zebrafish were exposed to 100 and 1000 µg/l PM for 7 days to assess its effects on metabolism and the gut microbiota. We observed a significant decrease in triglyceride (TG) in the livers of zebrafish that were exposed to 1000 µg/l PM for 7 days. At the same time, some genes related to glycolysis and lipid metabolism in the livers of zebrafish, including hexokinase-1 (HK1), pyruvate kinase (PK), acyl-CoA oxidase (Aco), peroxisome proliferator activated receptor alpha (Ppar-α), apolipoprotein A-IV-like (Apo), Acetyl CoA carboxylase-1 (Acc1), diacylglycerol acyltransferase (Dgat), and fatty acid synthase (Fas), were also decreased significantly after PM exposure. Based on GC-MS metabolomics analysis, a total of 48 metabolites changed significantly in the 1000 µg/l PM treatment group in comparison with the control group. These altered metabolites were mainly associated with the glycolysis, amino acid metabolism, and lipid metabolism pathways. Interestingly, we further found that the 1000 µg/l PM treatment group also showed significant elevations in Proteobacteria, Bacteroidetes, and Firmicutes at the phylum level. Sequencing of the 16S rRNA gene in the V3-V4 region also showed a significant change in the abundance and diversity of the gut microbiota in the 1000 µg/l PM treatment group. Our results indicated that exposure to PM for a short time could induce hepatic metabolic disorders and gut microbiota dysbiosis in adult male zebrafish.


Assuntos
Carbamatos/toxicidade , Disbiose/fisiopatologia , Microbioma Gastrointestinal/efeitos dos fármacos , Fígado/efeitos dos fármacos , Doenças Metabólicas/fisiopatologia , Animais , Bactérias/classificação , Bactérias/genética , Disbiose/induzido quimicamente , Disbiose/genética , Microbioma Gastrointestinal/genética , Microbioma Gastrointestinal/fisiologia , Expressão Gênica/efeitos dos fármacos , Fígado/metabolismo , Fígado/patologia , Masculino , Doenças Metabólicas/induzido quimicamente , Doenças Metabólicas/genética , Metabolômica/métodos , RNA Ribossômico 16S/genética , Transdução de Sinais/efeitos dos fármacos , Transdução de Sinais/genética , Fatores de Tempo , Testes de Toxicidade , Peixe-Zebra
14.
Lab Anim ; 53(3): 271-280, 2019 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-30580671

RESUMO

The world-wide incidence of many immune-mediated and metabolic diseases, including those of the intestines and liver, is steadily increasing. Gut microbiota plays a central role in the pathogenesis of these diseases as it mediates environmental changes to the intestinal immune system. Various environmental factors including diet, food additives and medication also trigger the compositional and functional alterations of microbiota, that is, dysbiosis, and this dysbiosis is closely associated with many chronic inflammatory diseases. However, the causal relationship remains unclear for the majority of these diseases. In this review, we discuss essential epidemiological data, known pathogenetic factors including those of genetic and environmental nature, while mainly focusing on the role of gut microbiota in the development of selected intestinal and liver diseases. Using specific examples, we also briefly describe some of the most widely-used animal models including gnotobiotic models and their contribution to the research of pathogenetic mechanisms of the host-microbiota relationship.


Assuntos
Disbiose/fisiopatologia , Microbioma Gastrointestinal/fisiologia , Vida Livre de Germes/fisiologia , Enteropatias/fisiopatologia , Hepatopatias/fisiopatologia , Animais , Modelos Animais de Doenças , Disbiose/microbiologia , Enteropatias/microbiologia , Hepatopatias/microbiologia , Camundongos
15.
Nutr Hosp ; 35(6): 1432-1440, 2018 Dec 03.
Artigo em Inglês | MEDLINE | ID: mdl-30525859

RESUMO

INTRODUCTION: diet plays a decisive role in the prevention and treatment of diseases such as obesity, diabetes, allergies and inflammatory diseases. In addition to this, there are numerous investigations about the role of the microbiota in the genesis of metabolic diseases, especially obesity and its comorbidities. OBJECTIVE: the aim of this review is to discuss the influence of high-fat diets on dysbiosis and metabolic endotoxemia. RESULTS AND CONCLUSION: the intestinal microbial ecosystem has been shown to be essential in the performance of functions in the host organism, however, several factors can lead to an imbalance in the homeostasis of the microbiota, known as dysbiosis. High-fat diets are associated with a reduction in intestinal bacterial diversity, changes in membrane integrity, inducing increased permeability and increased lipopolysaccharide (LPS) translocation, changes in the immune system, and generation of low-intensity systemic inflammation. The installed endotoxemia can be considered as a causal factor of subclinical inflammation related to several chronic diseases, and as a result of this, it is essential to know the real impact of hyperlipidic diets on the intestinal microbiota. Thus, it becomes essential to identify dietary strategies that can minimize the inflammatory effects generated from changes in the intestinal microbiota.


Assuntos
Dieta Hiperlipídica/efeitos adversos , Disbiose/etiologia , Endotoxemia/etiologia , Animais , Disbiose/patologia , Disbiose/fisiopatologia , Endotoxemia/patologia , Endotoxemia/fisiopatologia , Feminino , Microbioma Gastrointestinal/fisiologia , Humanos , Intestinos/patologia , Intestinos/fisiopatologia , MEDLINE , Masculino , Camundongos
16.
Nutr. hosp ; 35(6): 1432-1440, nov.-dic. 2018. tab, graf
Artigo em Inglês | IBECS | ID: ibc-181486

RESUMO

Introduction: diet plays a decisive role in the prevention and treatment of diseases such as obesity, diabetes, allergies and inflammatory diseases. In addition to this, there are numerous investigations about the role of the microbiota in the genesis of metabolic diseases, especially obesity and its comorbidities. Objective: the aim of this review is to discuss the influence of high-fat diets on dysbiosis and metabolic endotoxemia. Results and conclusion: the intestinal microbial ecosystem has been shown to be essential in the performance of functions in the host organism, however, several factors can lead to an imbalance in the homeostasis of the microbiota, known as dysbiosis. High-fat diets are associated with a reduction in intestinal bacterial diversity, changes in membrane integrity, inducing increased permeability and increased lipopolysaccharide (LPS) translocation, changes in the immune system, and generation of low-intensity systemic inflammation. The installed endotoxemia can be considered as a causal factor of subclinical inflammation related to several chronic diseases, and as a result of this, it is essential to know the real impact of hyperlipidic diets on the intestinal microbiota. Thus, it becomes essential to identify dietary strategies that can minimize the inflammatory effects generated from changes in the intestinal microbiota


Introducción: la dieta juega un papel determinante en la prevención y el tratamiento de enfermedades como la obesidad, la diabetes, las alergias y las enfermedades inflamatorias. Agregado a ello, son innumerables las investigaciones acerca del papel de la microbiota en la génesis de las enfermedades metabólicas, principalmente la obesidad y sus comorbilidades. Objetivo: el objetivo de esta revisión es analizar la influencia de las dietas ricas en grasas sobre la disbiosis y la endotoxemia metabólica. Resultados y conclusión: se ha demostrado que el ecosistema microbiano intestinal es esencial en el desempeño de funciones en el organismo del huésped, sin embargo, varios factores pueden conducir a un desequilibrio en la homeostasis de la microbiota, conocido como disbiosis. Las dietas ricas en grasas están asociadas a una reducción en la diversidad bacteriana intestinal, alteraciones en la integridad de la membrana que inducen un aumento de la permeabilidad y mayor translocación de lipopolisacáridos (LPS), alteraciones en el sistema inmunológico y generación de inflamación sistémica de baja intensidad. La endotoxemia instalada puede ser considerada un factor causal de la inflamación subclínica relacionada con diversas enfermedades crónicas y, en consecuencia, es imprescindible el conocimiento del impacto real de las dietas hiperlipídicas sobre la microbiota intestinal. Así, es esencial la identificación de estrategias dietéticas que puedan minimizar los efectos inflamatorios generados a partir de alteraciones en la microbiota intestinal


Assuntos
Humanos , Masculino , Feminino , Camundongos , Dieta Hiperlipídica/efeitos adversos , Disbiose/etiologia , Endotoxemia/etiologia , Disbiose/patologia , Disbiose/fisiopatologia , Endotoxemia/patologia , Endotoxemia/fisiopatologia , Microbioma Gastrointestinal/fisiologia , Intestinos/patologia , Intestinos/fisiopatologia , MEDLINE
17.
World J Gastroenterol ; 24(34): 3813-3820, 2018 Sep 14.
Artigo em Inglês | MEDLINE | ID: mdl-30228776

RESUMO

Cirrhosis is an increasing cause of morbidity and mortality. Recent studies are trying to clarify the role of microbiome in clinical exacerbation of patients with decompensated cirrhosis. Nowadays, it is accepted that patients with cirrhosis have altered salivary and enteric microbiome, characterized by the presence of dysbiosis. This altered microbiome along with small bowel bacterial overgrowth, through translocation across the gut, is associated with the development of decompensating complications. Studies have analyzed the correlation of certain bacterial families with the development of hepatic encephalopathy in cirrhotics. In general, stool and saliva dysbiosis with reduction of autochthonous bacteria in patients with cirrhosis incites changes in bacterial defenses and higher risk for bacterial infections, such as spontaneous bacterial peritonitis, and sepsis. Gut microbiome has even been associated with oncogenic pathways and under circumstances might promote the development of hepatocarcinogenesis. Lately, the existence of the oral-gut-liver axis has been related with the development of decompensating events. This link between the liver and the oral cavity could be via the gut through impaired intestinal permeability that allows direct translocation of bacteria from the oral cavity to the systemic circulation. Overall, the contribution of the microbiome to pathogenesis becomes more pronounced with progressive disease and therefore may represent an important therapeutic target in the management of cirrhosis.


Assuntos
Disbiose/fisiopatologia , Microbioma Gastrointestinal/fisiologia , Encefalopatia Hepática/fisiopatologia , Cirrose Hepática/fisiopatologia , Progressão da Doença , Disbiose/microbiologia , Encefalopatia Hepática/microbiologia , Humanos , Intestinos/microbiologia , Fígado/microbiologia , Fígado/fisiopatologia , Cirrose Hepática/microbiologia , Peritonite/epidemiologia , Peritonite/imunologia , Peritonite/microbiologia , Prevalência , Sepse/epidemiologia , Sepse/imunologia , Sepse/microbiologia
18.
Postgrad Med J ; 94(1114): 446-452, 2018 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-30026389

RESUMO

BACKGROUND: The gut-brain axis facilitates a critical bidirectional link and communication between the brain and the gut. Recent studies have highlighted the significance of interactions in the gut-brain axis, with a particular focus on intestinal functions, the nervous system and the brain. Furthermore, researchers have examined the effects of the gut microbiome on mental health and psychiatric well-being.The present study reviewed published evidence to explore the concept of the gut-brain axis. AIMS: This systematic review investigated the relationship between human brain function and the gut-brain axis. METHODS: To achieve these objectives, peer-reviewed articles on the gut-brain axis were identified in various electronic databases, including PubMed, MEDLINE, CIHAHL, Web of Science and PsycINFO. RESULTS: Data obtained from previous studies showed that the gut-brain axis links various peripheral intestinal functions to brain centres through a broad range of processes and pathways, such as endocrine signalling and immune system activation. Researchers have found that the vagus nerve drives bidirectional communication between the various systems in the gut-brain axis. In humans, the signals are transmitted from the liminal environment to the central nervous system. CONCLUSIONS: The communication that occurs in the gut-brain axis can alter brain function and trigger various psychiatric conditions, such as schizophrenia and depression. Thus, elucidation of the gut-brain axis is critical for the management of certain psychiatric and mental disorders.


Assuntos
Sistema Nervoso Central/fisiopatologia , Disbiose/fisiopatologia , Microbioma Gastrointestinal , Trato Gastrointestinal/fisiopatologia , Transtornos Mentais/microbiologia , Transtornos Mentais/fisiopatologia , Humanos
19.
Nutrients ; 10(6)2018 Jun 01.
Artigo em Inglês | MEDLINE | ID: mdl-29857583

RESUMO

In recent years evidence has emerged that neurodegenerative diseases (NDs) are strongly associated with the microbiome composition in the gut. Parkinson's disease (PD) is the most intensively studied neurodegenerative disease in this context. In this review, we performed a systematic evaluation of the published literature comparing changes in colonic microbiome in PD to the ones observed in other NDs including Alzheimer's disease (AD), multiple system atrophy (MSA), multiple sclerosis (MS), neuromyelitis optica (NMO) and amyotrophic lateral sclerosis (ALS). To enhance the comparability of different studies, only human case-control studies were included. Several studies showed an increase of Lactobacillus, Bifidobacterium, Verrucomicrobiaceae and Akkermansia in PD. A decrease of Faecalibacterium spp., Coprococcus spp., Blautia spp., Prevotella spp. and Prevotellaceae was observed in PD. On a low taxonomic resolution, like the phylum level, the changes are not disease-specific and are inconsistent. However, on a higher taxonomic resolution like genus or species level, a minor overlap was observed between PD and MSA, both alpha synucleinopathies. We show that standardization of sample collection and analysis is necessary for ensuring the reproducibility and comparability of data. We also provide evidence that assessing the microbiota composition at high taxonomic resolution reveals changes in relative abundance that may be specific to or characteristic of one disease or disease group, and might evolve discriminative power. The interactions between bacterial species and strains and the co-abundances must be investigated before assumptions about the effects of specific bacteria on the host can be made with certainty.


Assuntos
Disbiose/microbiologia , Sistema Nervoso Entérico/fisiopatologia , Medicina Baseada em Evidências , Microbioma Gastrointestinal , Mucosa Intestinal/microbiologia , Neuroimunomodulação , Doença de Parkinson/microbiologia , Pesquisa Biomédica/métodos , Fatores de Confusão (Epidemiologia) , Progressão da Doença , Disbiose/epidemiologia , Disbiose/imunologia , Disbiose/fisiopatologia , Sistema Nervoso Entérico/imunologia , Microbioma Gastrointestinal/imunologia , Humanos , Mucosa Intestinal/imunologia , Mucosa Intestinal/inervação , Mucosa Intestinal/fisiopatologia , Doenças Neurodegenerativas/epidemiologia , Doenças Neurodegenerativas/imunologia , Doenças Neurodegenerativas/microbiologia , Doenças Neurodegenerativas/fisiopatologia , Doença de Parkinson/epidemiologia , Doença de Parkinson/imunologia , Doença de Parkinson/fisiopatologia , Reprodutibilidade dos Testes , Projetos de Pesquisa , Índice de Gravidade de Doença
20.
Diabetes ; 67(8): 1512-1523, 2018 08.
Artigo em Inglês | MEDLINE | ID: mdl-29793999

RESUMO

Altering the gut microbiome may be beneficial to the host and recently arose as a promising strategy to manage obesity. Here, we investigated the relative contribution of ω3 polyunsaturated fatty acid (PUFA)-mediated alterations in the microbiota to metabolic parameter changes in mice. Four groups were compared: male fat-1 transgenic mice (with constitutive production of ω3 PUFAs) and male wild-type (WT) littermates fed an obesogenic (high fat/high sucrose [HFHS]) or a control diet. Unlike WT mice, HFHS-fed fat-1 mice were protected against obesity, glucose intolerance, and hepatic steatosis. Unlike WT mice, fat-1 mice maintained a normal barrier function, resulting in a significantly lower metabolic endotoxemia. The fat-1 mice displayed greater phylogenic diversity in the cecum, and fecal microbiota transplantation from fat-1 to WT mice was able to reverse weight gain and to normalize glucose tolerance and intestinal permeability. We concluded that the ω3 PUFA-mediated alteration of gut microbiota contributed to the prevention of metabolic syndrome in fat-1 mice. It occurred independently of changes in the PUFA content of host tissues and may represent a promising strategy to prevent metabolic disease and preserve a lean phenotype.


Assuntos
Ácidos Graxos Ômega-3/metabolismo , Transplante de Microbiota Fecal , Microbioma Gastrointestinal , Intolerância à Glucose/prevenção & controle , Resistência à Insulina , Hepatopatia Gordurosa não Alcoólica/prevenção & controle , Obesidade/prevenção & controle , Animais , Caderinas/genética , Caderinas/metabolismo , Dieta da Carga de Carboidratos/efeitos adversos , Dieta Hiperlipídica/efeitos adversos , Sacarose na Dieta/efeitos adversos , Disbiose/microbiologia , Disbiose/fisiopatologia , Disbiose/terapia , Endotoxemia/etiologia , Endotoxemia/prevenção & controle , Transplante de Microbiota Fecal/efeitos adversos , Intolerância à Glucose/microbiologia , Intolerância à Glucose/patologia , Intolerância à Glucose/fisiopatologia , Mucosa Intestinal/metabolismo , Mucosa Intestinal/microbiologia , Mucosa Intestinal/patologia , Mucosa Intestinal/fisiopatologia , Intestinos/microbiologia , Intestinos/patologia , Intestinos/fisiopatologia , Fígado/metabolismo , Fígado/patologia , Masculino , Camundongos Transgênicos , Músculo Esquelético/metabolismo , Hepatopatia Gordurosa não Alcoólica/microbiologia , Hepatopatia Gordurosa não Alcoólica/patologia , Hepatopatia Gordurosa não Alcoólica/fisiopatologia , Obesidade/microbiologia , Obesidade/patologia , Obesidade/fisiopatologia , Permeabilidade , Filogenia
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