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2.
Molecules ; 25(15)2020 Jul 22.
Artigo em Inglês | MEDLINE | ID: mdl-32707945

RESUMO

Vitamin B3, or niacin, is one of the most important compounds of the B-vitamin complex. Recent reports have demonstrated the involvement of vitamin B3 in a number of pivotal functions which ensure that homeostasis is maintained. In addition, the intriguing nature of its synthesis and the underlying mechanism of action of vitamin B3 have encouraged further studies aimed at deepening our understanding of the close link between the exogenous supply of B3 and how it activates dependent enzymes. This crucial role can be attributed to the gut microflora and its ability to shape human behavior and development by mediating the bioavailability of metabolites. Recent studies have indicated a possible interconnection between the novel coronavirus and commensal bacteria. As such, we have attempted to explain how the gastrointestinal deficiencies displayed by SARS-CoV-2-infected patients arise. It seems that the stimulation of a proinflammatory cascade and the production of large amounts of reactive oxygen species culminates in the subsequent loss of host eubiosis. Studies of the relationhip between ROS, SARS-CoV-2, and gut flora are sparse in the current literature. As an integrated component, oxidative stress (OS) has been found to negatively influence host eubiosis, in vitro fertilization outcomes, and oocyte quality, but to act as a sentinel against infections. In conclusion, research suggests that in the future, a healthy diet may be considered a reliable tool for maintaining and optimizing our key internal parameters.


Assuntos
Infecções por Coronavirus/patologia , Microbioma Gastrointestinal/fisiologia , Niacina/metabolismo , Niacinamida/metabolismo , Estresse Oxidativo/fisiologia , Pneumonia Viral/patologia , Betacoronavirus/metabolismo , Disbiose/fisiopatologia , Humanos , Pandemias , Espécies Reativas de Oxigênio/metabolismo
3.
Nature ; 583(7816): 441-446, 2020 07.
Artigo em Inglês | MEDLINE | ID: mdl-32641826

RESUMO

Connections between the gut and brain monitor the intestinal tissue and its microbial and dietary content1, regulating both physiological intestinal functions such as nutrient absorption and motility2,3, and brain-wired feeding behaviour2. It is therefore plausible that circuits exist to detect gut microorganisms and relay this information to areas of the central nervous system that, in turn, regulate gut physiology4. Here we characterize the influence of the microbiota on enteric-associated neurons by combining gnotobiotic mouse models with transcriptomics, circuit-tracing methods and functional manipulations. We find that the gut microbiome modulates gut-extrinsic sympathetic neurons: microbiota depletion leads to increased expression of the neuronal transcription factor cFos, and colonization of germ-free mice with bacteria that produce short-chain fatty acids suppresses cFos expression in the gut sympathetic ganglia. Chemogenetic manipulations, translational profiling and anterograde tracing identify a subset of distal intestine-projecting vagal neurons that are positioned to have an afferent role in microbiota-mediated modulation of gut sympathetic neurons. Retrograde polysynaptic neuronal tracing from the intestinal wall identifies brainstem sensory nuclei that are activated during microbial depletion, as well as efferent sympathetic premotor glutamatergic neurons that regulate gastrointestinal transit. These results reveal microbiota-dependent control of gut-extrinsic sympathetic activation through a gut-brain circuit.


Assuntos
Microbioma Gastrointestinal/fisiologia , Intestinos/inervação , Neurônios/fisiologia , Sistema Nervoso Simpático/citologia , Sistema Nervoso Simpático/fisiologia , Animais , Disbiose/fisiopatologia , Feminino , Gânglios Simpáticos/citologia , Gânglios Simpáticos/fisiologia , Motilidade Gastrointestinal , Vida Livre de Germes , Intestinos/microbiologia , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Modelos Animais , Vias Neurais/fisiologia , Proteínas Proto-Oncogênicas c-fos/metabolismo , Transcriptoma
4.
Brain Nerve ; 72(3): 241-250, 2020 Mar.
Artigo em Japonês | MEDLINE | ID: mdl-32152257

RESUMO

Dysregulation of the gut microbiome is associated with several life-threatening conditions, and might therefore represent a useful target for the prevention of dementia. However, the relationship between the gut microbiome and dementia has not yet been fully elucidated. Here, we recruited outpatients visiting our memory clinic to participate in this study. Information for patient demographics, various risk factors, and daily activities was collected, and cognitive function was assessed using neuropsychological tests and magnetic resonance imaging scans. Fecal samples were obtained, and the gut microbiome was assessed by terminal restriction fragment length polymorphism (T-RFLP) analysis, one of the most well-established and reliable 16S ribosomal RNA-based methods for classifying gut microbiota. Multivariable logistic regression models were used to identify factors independently associated with dementia and mild cognitive impairment. Graphical modelling was used to illustrate mutual associations. We analyzed 128 eligible patients (female: 59%, mean age: 74.2±8.7 years, mean Mini Mental State Examination score 24). Multivariable analyses showed that enterotype I and enterotype III bacteria were strongly associated with dementia, independent of traditional dementia biomarkers. Further studies investigating metabolites of gut microbes are needed to determine the mechanism underlying this association.


Assuntos
Cognição , Demência/microbiologia , Disbiose/fisiopatologia , Microbioma Gastrointestinal , Idoso , Idoso de 80 Anos ou mais , Bactérias/classificação , Fezes/microbiologia , Feminino , Humanos , Masculino , RNA Ribossômico 16S/genética
5.
Curr Gastroenterol Rep ; 22(2): 8, 2020 Jan 30.
Artigo em Inglês | MEDLINE | ID: mdl-32002666

RESUMO

PURPOSE OF REVIEW: The bidirectional relationship between sleep disorders and inflammatory bowel disease (IBD) has gained considerable attention in recent years. It has been suggested that poor sleep and fatigue are extra-intestinal manifestations of IBD. This review reports recent studies exploring subjective and objective assessments of sleep in the adult IBD population. RECENT FINDINGS: In ulcerative colitis patients, poor sleep has been independently linked to depression and poorer IBD-related quality of life. Using home polysomnography, IBD patients were shown to have less rapid eye movement sleep and Crohn's patient had increased lighter sleep. A study utilizing surveys assessing circadian rhythms described circadian misalignment in IBD patients and reported that circadian misalignment in Crohn's disease was associated with a more aggressive disease phenotype. The use of biologics may improve sleep disturbances in patients with IBD. Translational and clinical studies have reported that disturbances in sleep quality are linked to intestinal inflammation and a heighted systemic immune response. IBD patients appear to have disturbed sleep. Poor sleep is also suggested as a marker for subclinical disease activity. Recent studies have suggested circadian misalignment in IBD patients, and future studies are needed to assess these clinical implications.


Assuntos
Fadiga/etiologia , Doenças Inflamatórias Intestinais/complicações , Transtornos do Sono-Vigília/etiologia , Produtos Biológicos/uso terapêutico , Ritmo Circadiano/fisiologia , Disbiose/fisiopatologia , Fadiga/tratamento farmacológico , Fadiga/fisiopatologia , Humanos , Inflamação/fisiopatologia , Doenças Inflamatórias Intestinais/tratamento farmacológico , Doenças Inflamatórias Intestinais/fisiopatologia , Polissonografia , Transtornos do Sono-Vigília/diagnóstico , Transtornos do Sono-Vigília/tratamento farmacológico , Transtornos do Sono-Vigília/fisiopatologia
6.
Gut ; 69(3): 513-522, 2020 03.
Artigo em Inglês | MEDLINE | ID: mdl-31900289

RESUMO

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 Fusobacterium and Veillonella, were enriched, whereas beneficial bacteria, including Faecalibacterium and Akkermansia, 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, Fusobacterium, 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.


Assuntos
Translocação Bacteriana , Disbiose/complicações , Microbioma Gastrointestinal , Placenta/imunologia , Placenta/microbiologia , Pré-Eclâmpsia/microbiologia , Animais , Pressão Sanguínea , Contagem de Linfócito CD4 , Estudos de Casos e Controles , Quimiocinas/genética , Creatinina/sangue , Citocinas/genética , Modelos Animais de Doenças , Disbiose/fisiopatologia , Faecalibacterium , Fezes/microbiologia , Feminino , Reabsorção do Feto/microbiologia , Fusobactérias , Humanos , Intestino Delgado/imunologia , Camundongos , Placenta/metabolismo , Pré-Eclâmpsia/fisiopatologia , Gravidez , Proteinúria/urina , RNA Mensageiro/metabolismo , Linfócitos T Reguladores , Células Th17 , Veillonella
7.
Artigo em Inglês | MEDLINE | ID: mdl-31973090

RESUMO

Alcohol-related disorders (ARD) are highly prevalent among Latin American-Caribbean countries. Mental disorders are common comorbidities in individuals with ARD. However, the etiology of the association between ARD and mental disorders remains unclear. We examined the association of inflammatory cytokines, microbiome, and other biomakers with measures of depression, social anxiety, and executive functions. We observed a significant increase in cytokine and chemokine expression levels in saliva and plasma in the alcohol group (AG) samples. Also, the salivary bacterial composition in the AG revealed an abundance of Prevotella. Depression symptomatology was markedly higher in the AG, but social anxiety levels were negligible. AG also exhibited executive dysfunctions, which negatively correlated with increased plasma levels of pro-inflammatory cytokines and increased salivary concentrations of Prevotella bacteria. Our study suggests that chronic alcohol use correlates with executive dysfunction, immune system dysregulation, and dysbiosis of the salivary microbiota. Additional studies are needed to understand the role of the microbiome and inflammation in alcohol use and mental comorbidities.


Assuntos
Consumo de Bebidas Alcoólicas/efeitos adversos , Depressão/epidemiologia , Função Executiva , Inflamação/epidemiologia , Transtornos Mentais/epidemiologia , Microbiota , Adulto , Transtornos Relacionados ao Uso de Álcool , Biomarcadores/análise , Disbiose/fisiopatologia , Feminino , Humanos , Sistema Imunitário/fisiopatologia , Masculino , Pessoa de Meia-Idade , Saliva/química , Adulto Jovem
8.
Gut ; 69(3): 591-600, 2020 03.
Artigo em Inglês | MEDLINE | ID: mdl-31784469

RESUMO

Emerging data increasingly point towards the duodenum as a key region underlying the pathophysiology of functional dyspepsia (FD), one of the most prevalent functional GI disorders. The duodenum plays a major role in the control and coordination of gastroduodenal function. Impaired duodenal mucosal integrity and low-grade inflammation have been associated with altered neuronal signalling and systemic immune activation, and these alterations may ultimately lead to dyspeptic symptoms. Likely luminal candidates inducing the duodenal barrier defect include acid, bile, the microbiota and food antigens although no causal association with symptoms has been convincingly demonstrated. Recognition of duodenal pathology in FD will hopefully lead to the discovery of new biomarkers and therapeutic targets, allowing biologically targeted rather than symptom-based therapy. In this review, we summarise the recent advances in the diagnosis and treatment of FD with a focus on the duodenum.


Assuntos
Duodeno/fisiopatologia , Dispepsia/tratamento farmacológico , Dispepsia/etiologia , Antibacterianos/uso terapêutico , Ácidos e Sais Biliares/metabolismo , Encéfalo/fisiopatologia , Duodeno/imunologia , Duodeno/metabolismo , Duodeno/microbiologia , Disbiose/tratamento farmacológico , Disbiose/fisiopatologia , Dispepsia/diagnóstico , Dispepsia/fisiopatologia , Esvaziamento Gástrico , Humanos , Neurotransmissores/uso terapêutico , Probióticos/uso terapêutico , Inibidores da Bomba de Prótons/uso terapêutico
9.
Artigo em Inglês | MEDLINE | ID: mdl-31809363

RESUMO

BACKGROUND: The intestinal microbiota contributes to the pathogenesis of obesity and metabolic disorders. People living with HIV (PLWH) have a higher risk for the development of visceral adiposity with accompanying worsened cardiovascular risk. SETTING: Convenience sample from an HIV clinic and research unit. METHODS: To understand the relationship between adiposity and intestinal dysbiosis, we compared the gut microbiota and inflammatory markers in a cross-sectional study of viscerally obese, generally obese, and lean PLWH. Fecal intestinal microbiota was characterized by 16S ribosomal DNA sequencing. Abdominal CTs quantified subcutaneous adipose tissue and visceral adipose tissue (SAT; VAT). Serum high sensitivity C-reactive protein, adiponectin, leptin, IL-6, MCP-1, and sCD14 were assayed. RESULTS: We studied 15, 9, and 11 participants with visceral obesity, general obesity, and lean body type, respectively. The generally obese group were all women and 2/3 African American, whereas the visceral obesity and lean groups were predominantly white and men who have sex with men. Markers of systemic inflammation and sCD14 were higher in general obesity compared with lean. sCD14 was positively correlated with VAT, but not SAT. Bacterial diversity was significantly reduced in participants with visceral and general obesity and composition of intestinal microbiota was significantly different from lean body types. Bacterial alpha diversity was negatively correlated with VAT area, waist/hip ratio, and sCD14, but not with SAT area. CONCLUSIONS: In this exploratory study, obesity in general was associated with dysbiotic intestinal microbiota. The relationships of VAT to bacterial diversity and sCD14 suggest that dysbiosis in viscerally obese PLWH could be associated with heightened inflammatory state.


Assuntos
Biomarcadores/metabolismo , Disbiose/fisiopatologia , Infecções por HIV/metabolismo , Inflamação/metabolismo , Gordura Intra-Abdominal/metabolismo , Obesidade/metabolismo , Adulto , Estudos Transversais , Feminino , Humanos , Masculino
10.
Biomed Res Int ; 2019: 9726786, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31886272

RESUMO

Although gut dysbiosis appears in 20%-75% of cirrhotic patients, there are limited data on microbiota profiles in viral hepatitis cirrhotics and its role in progression to cirrhosis. Further understanding on the relationship between gut dysbiosis and cirrhosis presents a unique opportunity in not only predicting the development of cirrhosis but also discovering new therapies. Recent advances have been made on identifying unique microbiota in viral hepatitis cirrhotics and adopting the microbiota index to predict cirrhosis. Therapeutic intervention with microbiome-modulating has been explored. Cirrhosis from viral infection has unique bacterial or fungal profiles, which include increased numbers of Prevotella, Streptococcus, Staphylococcaceae, and Enterococcus, as well as decreased Ruminococcus and Clostridium. In addition, the gut microbiota can stimulate liver immunity, effectively helping hepatitis virus clearance. In clinical settings, CDR, GDI, Basidiomycota/Ascomycota, specific POD, and so forth are efficient microbiota indexes to diagnose or prognosticate cirrhosis from viral hepatitis. FMT, probiotics, and prebiotics can restore microbial diversity in cirrhotic patients with viral hepatitis, decrease ammonia serum or endotoxemia levels, prevent complications, reduce rehospitalization rate, and improve prognosis. Cirrhotics from viral hepatitis had unique bacterial or fungal profiles, associated with specific metabolic, immune, and endocrinological statuses. Such profiles are modifiable with medical treatment. The role of gut archaea and virome, implementation of FMT, microbiota metabolites as adjuvant immunotherapy, and microbiota indexes for prognostication deserve attention.


Assuntos
Disbiose , Microbioma Gastrointestinal , Hepatite , Cirrose Hepática , Disbiose/fisiopatologia , Disbiose/virologia , Humanos , Fígado/fisiologia , Fígado/virologia , Cirrose Hepática/fisiopatologia , Cirrose Hepática/virologia
11.
Nutrients ; 11(11)2019 Nov 09.
Artigo em Inglês | MEDLINE | ID: mdl-31717475

RESUMO

As food is an active subject and may have anti-inflammatory or pro-inflammatory effects, dietary habits may modulate the low-grade neuroinflammation associated with chronic neurodegenerative diseases. Food is living matter different from us, but made of our own nature. Therefore, it is at the same time foreign to us (non-self), if not yet digested, and like us (self), after its complete digestion. To avoid the efflux of undigested food from the lumen, the intestinal barrier must remain intact. What and how much we eat shape the composition of gut microbiota. Gut dysbiosis, as a consequence of Western diets, leads to intestinal inflammation and a leaky intestinal barrier. The efflux of undigested food, microbes, endotoxins, as well as immune-competent cells and molecules, causes chronic systemic inflammation. Opening of the blood-brain barrier may trigger microglia and astrocytes and set up neuroinflammation. We suggest that what determines the organ specificity of the autoimmune-inflammatory process may depend on food antigens resembling proteins of the organ being attacked. This applies to the brain and neuroinflammatory diseases, as to other organs and other diseases, including cancer. Understanding the cooperation between microbiota and undigested food in inflammatory diseases may clarify organ specificity, allow the setting up of adequate experimental models of disease and develop targeted dietary interventions.


Assuntos
Dieta , Disbiose , Microbioma Gastrointestinal , Inflamação , Doenças Neurodegenerativas , Especificidade de Órgãos/imunologia , Animais , Transtorno Autístico/imunologia , Transtorno Autístico/microbiologia , Transtorno Autístico/fisiopatologia , Disbiose/imunologia , Disbiose/microbiologia , Disbiose/fisiopatologia , Humanos , Inflamação/imunologia , Inflamação/microbiologia , Inflamação/fisiopatologia , Camundongos , Doenças Neurodegenerativas/imunologia , Doenças Neurodegenerativas/microbiologia , Doenças Neurodegenerativas/fisiopatologia
12.
Int J Mol Sci ; 20(22)2019 Nov 08.
Artigo em Inglês | MEDLINE | ID: mdl-31717303

RESUMO

All over the world, there is an increase in the overall survival of the population and the number of elderly people. The incidence of allergic reactions is also rising worldwide. Until recently, allergies, and in particular food allergies (FAs), was regarded as a pediatric problem, since some of them start in early childhood and may spontaneously disappear in adulthood. It is being discovered that, on the contrary, these problems are increasingly affecting even the elderly. Along with other diseases that are considered characteristics of advanced age, such as cardiovascular, dysmetabolic, autoimmune, neurodegenerative, and oncological diseases, even FAs are increasingly frequent in the elderly. An FA is a pleiomorphic and multifactorial disease, characterized by an abnormal immune response and an impaired gut barrier function. The elderly exhibit distinct FA phenotypes, and diagnosis is difficult due to frequent co-morbidities and uncertainty in the interpretation of in vitro and in vivo tests. Several factors render the elderly susceptible to FAs, including the physiological changes of aging, a decline in gut barrier function, the skewing of adaptive immunity to a Th2 response, dysregulation of innate immune cells, and age-related changes of gut microbiota. Aging is accompanied by a progressive remodeling of immune system functions, leading to an increased pro-inflammatory status where type 1 cytokines are quantitatively dominant. However, serum Immunoglobulin E (IgE) levels and T helper type 2 (Th2 cytokine production have also been found to be increased in the elderly, suggesting that the type 2 cytokine pattern is not necessarily defective in older age. Dysfunctional dendritic cells in the gut, defects in secretory IgA, and decreased T regulatory function in the elderly also play important roles in FA development. We address herein the main immunologic aspects of aging according to the presence of FAs.


Assuntos
Envelhecimento/patologia , Hipersensibilidade Alimentar/patologia , Digestão , Disbiose/complicações , Disbiose/fisiopatologia , Epitélio/imunologia , Epitélio/patologia , Hipersensibilidade Alimentar/imunologia , Hipersensibilidade Alimentar/microbiologia , Hipersensibilidade Alimentar/fisiopatologia , Humanos , Sistema Imunitário/patologia , Sistema Imunitário/fisiopatologia
14.
Medicina (Kaunas) ; 55(8)2019 Aug 10.
Artigo em Inglês | MEDLINE | ID: mdl-31405111

RESUMO

The human microbiota is a variety of different microorganisms. The composition of microbiota varies from host to host, and it changes during the lifetime. It is known that microbiome may be changed because of a diet, bacteriophages and different processes for example, such as inflammation. Like all other areas of medicine, there is a continuous growth in the area of microbiology. Different microbes can reside in all sites of a human body, even in locations that were previously considered as sterile; for example, liver, pancreas, brain and adipose tissue. Presently one of the etiological factors for liver disease is considered to be pro-inflammatory changes in a host's organism. There are lot of supporting data about intestinal dysbiosis and increased intestinal permeability and its effect on development of liver disease pointing to the gut-liver axis. The gut-liver axis affects pathogenesis of many liver diseases, such as chronic hepatitis B, chronic hepatitis C, alcoholic liver disease, non-alcoholic liver disease, non-alcoholic steatohepatitis, liver cirrhosis and hepatocellular carcinoma. Gut microbiota has been implicated in the regulation of brain health, emphasizing the gut-brain axis. Also, experiments with mice showed that microorganisms have significant effects on the blood-brain barrier integrity. Microbiota can modulate a variety of mechanisms through the gut-liver axis and gut-brain axis. Normal intestinal flora impacts the health of a host in many positive ways, but there is now significant evidence that intestinal microbiota, especially altered, have the ability to impact the pathologies of many diseases through different inflammatory mechanisms. At this point, many of the pathophysiological reactions in case of microbial disbyosis are still unclear.


Assuntos
Microbioma Gastrointestinal/fisiologia , Microbiota/fisiologia , Disbiose/complicações , Disbiose/fisiopatologia , Humanos , Fígado/fisiologia , Cirrose Hepática/complicações , Cirrose Hepática/microbiologia , Cirrose Hepática/patologia
15.
Nutrients ; 11(8)2019 Aug 07.
Artigo em Inglês | MEDLINE | ID: mdl-31394758

RESUMO

Diet and microbiota each have a direct impact on many chronic, inflammatory, and metabolic diseases. As the field develops, a new perspective is emerging. The effects of diet may depend on the microbiota composition of the intestine. A diet that is rich in choline, red meat, dairy, or egg may promote the growth, or change the composition, of microbial species. The microbiota, in turn, may produce metabolites that increase the risk of cardiovascular disease. This article reviews our current understanding of the effects of the molecule trimethylamine-N-oxide (TMAO) obtained from food or produced by the microbiota. We review the mechanisms of actions of TMAO, and studies that associate it with cardiovascular and chronic kidney diseases. We introduce a novel concept: TMAO is one among a group of selective uremic toxins that may rise to high levels in the circulation or accumulate in various organs. Based on this information, we evaluate how TMAO may harm, by exacerbating inflammation, or may protect, by attenuating amyloid formation, in autoimmune diseases such as rheumatoid arthritis.


Assuntos
Artrite Reumatoide/fisiopatologia , Doenças Autoimunes/fisiopatologia , Dieta , Metilaminas/farmacologia , Microbiota/fisiologia , Amiloide/metabolismo , Animais , Doenças Cardiovasculares/etiologia , Disbiose/fisiopatologia , Intolerância à Glucose , Humanos , Inflamação/etiologia , Metilaminas/metabolismo , Insuficiência Renal Crônica , Fatores de Risco
16.
Int J Med Sci ; 16(6): 872-881, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31337961

RESUMO

Hypertension is the main risk factor for cerebral stroke and death resulting from cerebral stroke. Current association studies on hypertension and intestinal microbiota focus on patients with hypertension (HTN); however, no investigations involving patients with isolated diastolic hypertension (IDH) or systolic hypertension (SH) have been conducted to date. In this study, fecal samples from 62 cases with normal blood pressure (BP) and 67 cases with high BP were used for 16S amplicon sequencing. Sixty-one cases of HTN and 61 corresponding cases with normal BP were obtained by propensity score matching (PSM), and differential analysis was conducted using the DEseq2 package. PSM was also used to match six IDH patients with six controls and to match 35 cases of SH with 35 controls. There were 54 differential genera between the HTN and normal BP groups, and there were five differential genera between the IDH and normal BP groups. There were 38 differential genera between the SH and normal BP groups, including Christensenella. Bayesian network analysis showed that variations in BP influenced microbial abundance. Pearson's correlation analysis showed that bacterial abundance is correlated with BP. Significant differences between the intestinal microbiota of high and normal BP groups were observed. Gut microbiota dysbiosis differed among HTN, IDH, and SH patients. In particular, diastolic blood pressure (DBP) and systolic blood pressure (SBP) were related to different intestinal microbiota.


Assuntos
Pressão Sanguínea/fisiologia , Disbiose/microbiologia , Microbioma Gastrointestinal/fisiologia , Hipertensão/microbiologia , Idoso , Bactérias/isolamento & purificação , Determinação da Pressão Arterial , Estudos de Casos e Controles , Disbiose/fisiopatologia , Feminino , Humanos , Hipertensão/diagnóstico , Hipertensão/fisiopatologia , Masculino , Pessoa de Meia-Idade , Fatores de Risco
17.
Infect Immun ; 87(10)2019 10.
Artigo em Inglês | MEDLINE | ID: mdl-31308086

RESUMO

As important players in the host defense system, commensal microbes and the microbiota influence multiple aspects of host physiology. Bordetella pertussis infection is highly contagious among humans. However, the roles of the microbiota in B. pertussis pathogenesis are poorly understood. Here, we show that antibiotic-mediated depletion of the microbiota results in increased susceptibility to B. pertussis infection during the early stage. The increased susceptibility was associated with a marked impairment of the systemic IgG, IgG2a, and IgG1 antibody responses to B. pertussis infection after antibiotic treatment. Furthermore, the microbiota impacted the short-lived plasma cell responses as well as the recall responses of memory B cells to B. pertussis infection. Finally, we found that the dysbiosis caused by antibiotic treatment affects CD4+ T cell generation and PD-1 expression on CD4+ T cells and thereby perturbs plasma cell differentiation. Our results have revealed the importance of commensal microbes in modulating host immune responses to B. pertussis infection and support the possibility of controlling the severity of B. pertussis infection in humans by manipulating the microbiota.


Assuntos
Bordetella pertussis/imunologia , Disbiose/imunologia , Microbioma Gastrointestinal/imunologia , Imunidade Humoral , Simbiose/imunologia , Coqueluche/imunologia , Ampicilina/farmacologia , Animais , Antibacterianos/farmacologia , Anticorpos Antibacterianos/biossíntese , Anticorpos Antibacterianos/classificação , Bacteroidetes/classificação , Bacteroidetes/efeitos dos fármacos , Bacteroidetes/crescimento & desenvolvimento , Bacteroidetes/imunologia , Bordetella pertussis/crescimento & desenvolvimento , Bordetella pertussis/patogenicidade , Disbiose/microbiologia , Disbiose/fisiopatologia , Feminino , Firmicutes/classificação , Firmicutes/efeitos dos fármacos , Firmicutes/crescimento & desenvolvimento , Firmicutes/imunologia , Microbioma Gastrointestinal/efeitos dos fármacos , Imunidade Inata , Imunoglobulina G/biossíntese , Imunoglobulina G/classificação , Metronidazol/farmacologia , Camundongos , Camundongos Endogâmicos BALB C , Neomicina/farmacologia , Proteobactérias/classificação , Proteobactérias/efeitos dos fármacos , Proteobactérias/crescimento & desenvolvimento , Proteobactérias/imunologia , Simbiose/efeitos dos fármacos , Vancomicina/farmacologia , Coqueluche/microbiologia , Coqueluche/fisiopatologia
18.
Oxid Med Cell Longev ; 2019: 3086270, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31205584

RESUMO

The gut microbiota, the ecosystem formed by a wide symbiotic community of nonpathogenic microorganisms that are present in the distal part of the human gut, plays a prominent role in the normal physiology of the organism. The gut microbiota's imbalance, gut dysbiosis, is directly related to the origin of various processes of acute or chronic dysfunction in the host. Therefore, the ability to intervene in the gut microbiota is now emerging as a possible tactic for therapeutic intervention in various diseases. From this perspective, evidence is growing that a functional dietary intervention with probiotics, which maintain or restore beneficial bacteria of the digestive tract, represents a promising therapeutic strategy for interventions in cardiovascular diseases and also reduces the risk of their occurrence. In the present work, we review the importance of maintaining the balance of the intestinal microbiota to prevent or combat such processes as arterial hypertension or endothelial dysfunction, which underlie many cardiovascular disorders. We also review how the consumption of probiotics can improve autonomic control of cardiovascular function and provide beneficial effects in patients with heart failure. Among the known effects of probiotics is their ability to decrease the generation of reactive oxygen species and, therefore, reduce oxidative stress. Therefore, in this review, we specifically focus on this antioxidant capacity and its relationship with the beneficial cardiovascular effects described for probiotics.


Assuntos
Doenças Cardiovasculares/prevenção & controle , Suplementos Nutricionais , Disbiose/tratamento farmacológico , Microbioma Gastrointestinal/efeitos dos fármacos , Estresse Oxidativo/efeitos dos fármacos , Probióticos/uso terapêutico , Doenças Cardiovasculares/microbiologia , Disbiose/fisiopatologia , Trato Gastrointestinal/efeitos dos fármacos , Trato Gastrointestinal/microbiologia , Humanos
19.
Biomed Pharmacother ; 116: 109002, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31154270

RESUMO

Berberine (BBR) is a non-prescription drug to treat various bacteria-associated diarrheas. However, BBR has also been reported to cause diarrhea in clinic, with underlying mechanisms poorly understood. Because altered gut microbial ecology is a potential basis for diarrhea, this study was conducted to investigate the impact of BBR on gut microbiota of treatment-emergent diarrhea. BBR treatment (200 mg/kg, i.g.) in normal rats exhibited no significant changes in serum biochemical parameters but mild diarrhea occurred, accompanied with the decreased gastrointestinal transit time and increased fecal moisture, suggestive of the local effects of BBR in the intestine. Colon histology revealed the decreased abundance of mucus-filled goblet cells in BBR group. Although BBR-treated rats had the enlarged cecum with watery caecal digesta, short-chain fatty acids concentration was significantly lower than control group. Additionally, BBR caused gut microbiota dysbiosis by evaluating the decreased observed species number and Shannon index. BBR increased the relative abundances of families Porphyromonadaceae and Prevotellaceae as well as genera Parabacteroides, Prevotellaceae_UCG-001 and Prevotellaceae_NK3B31_group. Spearman's correlation analysis revealed family Prevotellaceae and genus Prevotellaceae_UCG-001 as the most prominent drivers of the BBR treatment-emergent diarrhea, correlating positively with fecal moisture but negatively with gastrointestinal transit time. This study therefore demonstrated that the treatment-emergent mild diarrhea of BBR was most likely due to the dysbiosis of the gut microbiota.


Assuntos
Berberina/efeitos adversos , Diarreia/induzido quimicamente , Diarreia/microbiologia , Disbiose/complicações , Disbiose/microbiologia , Microbioma Gastrointestinal , Animais , Biodiversidade , Ceco/patologia , Colo/efeitos dos fármacos , Colo/patologia , Colo/fisiopatologia , Diarreia/fisiopatologia , Disbiose/fisiopatologia , Ácidos Graxos/metabolismo , Fezes/química , Microbioma Gastrointestinal/efeitos dos fármacos , Trânsito Gastrointestinal/efeitos dos fármacos , Masculino , Tamanho do Órgão , Ratos Wistar , Estatísticas não Paramétricas
20.
Crit Care ; 23(1): 195, 2019 May 31.
Artigo em Inglês | MEDLINE | ID: mdl-31151471

RESUMO

BACKGROUND: Despite the essential functions of the intestinal microbiota in human physiology, little has been reported about the microbiome in neurocritically ill patients. This investigation aimed to evaluate the characteristics of the gut microbiome in neurocritically ill patients and its changes after admission. Furthermore, we investigated whether the characteristics of the gut microbiome at admission were a risk factor for death within 180 days. METHODS: This prospective observational cohort study included neurocritically ill patients admitted to the neurological intensive care unit of a large university-affiliated academic hospital in Guangzhou. Faecal samples were collected within 72 h after admission (before antibiotic treatment) and serially each week. Healthy volunteers were recruited from a community in Guangzhou. The gut microbiome was monitored via 16S rRNA gene sequence analysis, and the associations with the clinical outcome were evaluated by a Cox proportional hazards model. RESULTS: In total, 98 patients and 84 age- and sex-matched healthy subjects were included in the analysis. Compared with healthy subjects, the neurocritically ill patients exhibited significantly different compositions of intestinal microbiota. During hospitalization, the α-diversity and abundance of Ruminococcaceae and Lachnospiraceae decreased significantly over time in patients followed longitudinally. The abundance of Enterobacteriaceae was positively associated with the modified Rankin Scale at discharge. In the multivariate Cox regression analysis, Christensenellaceae and Erysipelotrichaceae were associated with an increased risk of death. The increases in intestinal Enterobacteriales and Enterobacteriaceae during the first week in the neurological intensive care unit were associated with increases of 92% in the risk of 180-day mortality after adjustments. CONCLUSIONS: This analysis of the gut microbiome in 98 neurocritically ill patients indicates that the gut microbiota composition in these patients differs significantly from that in a healthy population and that the magnitude of this dysbiosis increases during hospitalization in a neurological intensive care unit. The gut microbiota characteristics seem to have an impact on patients' 180-day mortality. Gut microbiota analysis could hopefully predict outcome in the future.


Assuntos
Disbiose/microbiologia , Microbioma Gastrointestinal/fisiologia , Doenças do Sistema Nervoso/complicações , Adulto , Idoso , China , Estudos de Coortes , Estado Terminal , Disbiose/etiologia , Disbiose/fisiopatologia , Fezes/microbiologia , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Doenças do Sistema Nervoso/fisiopatologia , Estudos Prospectivos , Estatísticas não Paramétricas
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