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1.
Nutrients ; 13(8)2021 Aug 03.
Artigo em Inglês | MEDLINE | ID: mdl-34444852

RESUMO

We aimed to observe the combined effects of Gaussian graphical model (GGM)-derived dietary patterns and the gastric microbiome on the risk of gastric cancer (GC) in a Korean population. The study included 268 patients with GC and 288 healthy controls. Food intake was assessed using a 106-item semiquantitative food frequency questionnaire. GGMs were applied to derive dietary pattern networks. 16S rRNA gene sequencing was performed using DNA extracted from gastric biopsy samples. The fruit pattern network was inversely associated with the risk of GC for the highest vs. lowest tertiles in the total population (odds ratio (OR): 0.47; 95% confidence interval (CI): 0.28-0.77; p for trend = 0.003) and in females (OR: 0.38; 95% CI: 0.17-0.83; p for trend = 0.021). Males who had a low microbial dysbiosis index (MDI) and high vegetable and seafood pattern score showed a significantly reduced risk of GC (OR: 0.44; 95% CI: 0.22-0.91; p-interaction = 0.021). Females who had a low MDI and high dairy pattern score showed a significantly reduced risk of GC (OR: 0.23; 95% CI: 0.07-0.76; p-interaction = 0.018). Our novel findings revealed that vegetable and seafood pattern might interact with dysbiosis to attenuate the risk of GC in males, whereas the dairy pattern might interact with dysbiosis to reduce the GC risk in females.


Assuntos
Dieta/efeitos adversos , Dieta/estatística & dados numéricos , Microbioma Gastrointestinal/fisiologia , Neoplasias Gástricas/etiologia , Estômago/microbiologia , Estudos de Casos e Controles , Inquéritos sobre Dietas , Disbiose/complicações , Disbiose/fisiopatologia , Ingestão de Alimentos/fisiologia , Feminino , Frutas , Humanos , Masculino , Pessoa de Meia-Idade , RNA Ribossômico 16S/análise , República da Coreia/epidemiologia , Fatores de Risco , Fatores Sexuais , Neoplasias Gástricas/epidemiologia , Neoplasias Gástricas/microbiologia , Verduras
2.
Nutrients ; 13(8)2021 Jul 27.
Artigo em Inglês | MEDLINE | ID: mdl-34444741

RESUMO

Gut microbiota has emerged as a major metabolically active organ with critical functions in both health and disease. The trillions of microorganisms hosted by the gastrointestinal tract are involved in numerous physiological and metabolic processes including modulation of appetite and regulation of energy in the host spanning from periphery to the brain. Indeed, bacteria and their metabolic byproducts are working in concert with the host chemosensory signaling pathways to affect both short- and long-term ingestive behavior. Sensing of nutrients and taste by specialized G protein-coupled receptor cells is important in transmitting food-related signals, optimizing nutrition as well as in prevention and treatment of several diseases, notably obesity, diabetes and associated metabolic disorders. Further, bacteria metabolites interact with specialized receptors cells expressed by gut epithelium leading to taste and appetite response changes to nutrients. This review describes recent advances on the role of gut bacteria in taste perception and functions. It further discusses how intestinal dysbiosis characteristic of several pathological conditions may alter and modulate taste preference and food consumption via changes in taste receptor expression.


Assuntos
Fenômenos Fisiológicos Bacterianos , Microbioma Gastrointestinal/fisiologia , Intestinos/microbiologia , Percepção Gustatória , Animais , Antineoplásicos/uso terapêutico , Cirurgia Bariátrica , COVID-19/fisiopatologia , Dieta , Disbiose/fisiopatologia , Comportamento Alimentar , Hormônios/metabolismo , Humanos , Doenças Inflamatórias Intestinais/fisiopatologia , Neoplasias/tratamento farmacológico , Neoplasias/fisiopatologia , Receptores Acoplados a Proteínas G/metabolismo , Paladar , Papilas Gustativas/fisiologia , Receptores Toll-Like/metabolismo
3.
Nutrients ; 13(6)2021 Jun 19.
Artigo em Inglês | MEDLINE | ID: mdl-34205336

RESUMO

Emerging evidence indicates that gut microbiota is important in the regulation of brain activity and cognitive functions. Microbes mediate communication among the metabolic, peripheral immune, and central nervous systems via the microbiota-gut-brain axis. However, it is not well understood how the gut microbiome and neurons in the brain mutually interact or how these interactions affect normal brain functioning and cognition. We summarize the mechanisms whereby the gut microbiota regulate the production, transportation, and functioning of neurotransmitters. We also discuss how microbiome dysbiosis affects cognitive function, especially in neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease.


Assuntos
Cognição/fisiologia , Microbioma Gastrointestinal/fisiologia , Doenças Neurodegenerativas/microbiologia , Neurotransmissores/fisiologia , Doença de Alzheimer/microbiologia , Animais , Ansiedade/microbiologia , Transtorno do Espectro Autista/microbiologia , Encéfalo/fisiopatologia , Depressão/microbiologia , Disbiose/fisiopatologia , Humanos , Doença de Parkinson/microbiologia , Esquizofrenia/microbiologia
4.
J Clin Invest ; 131(13)2021 07 01.
Artigo em Inglês | MEDLINE | ID: mdl-34196307

RESUMO

Neurodegenerative disorders (NDs) affect essential functions not only in the CNS, but also cause persistent gut dysfunctions, suggesting that they have an impact on both CNS and gut-innervating neurons. Although the CNS biology of NDs continues to be well studied, how gut-innervating neurons, including those that connect the gut to the brain, are affected by or involved in the etiology of these debilitating and progressive disorders has been understudied. Studies in recent years have shown how CNS and gut biology, aided by the gut-brain connecting neurons, modulate each other's functions. These studies underscore the importance of exploring the gut-innervating and gut-brain connecting neurons of the CNS and gut function in health, as well as the etiology and progression of dysfunction in NDs. In this Review, we discuss our current understanding of how the various gut-innervating neurons and gut physiology are involved in the etiology of NDs, including Parkinson's disease, Alzheimer's disease, Huntington's disease, and amyotrophic lateral sclerosis, to cause progressive CNS and persistent gut dysfunction.


Assuntos
Sistema Nervoso Entérico/fisiopatologia , Doenças Neurodegenerativas/etiologia , Doenças Neurodegenerativas/fisiopatologia , Doença de Alzheimer/etiologia , Doença de Alzheimer/fisiopatologia , Esclerose Amiotrófica Lateral/etiologia , Esclerose Amiotrófica Lateral/fisiopatologia , Animais , Encéfalo/fisiopatologia , Sistema Digestório/inervação , Sistema Digestório/fisiopatologia , Modelos Animais de Doenças , Progressão da Doença , Disbiose/fisiopatologia , Microbioma Gastrointestinal/fisiologia , Humanos , Doença de Huntington/etiologia , Doença de Huntington/fisiopatologia , Modelos Neurológicos , Mutação , Doenças Neurodegenerativas/microbiologia , Doença de Parkinson/etiologia , Doença de Parkinson/fisiopatologia
5.
J Clin Invest ; 131(13)2021 07 01.
Artigo em Inglês | MEDLINE | ID: mdl-34196310

RESUMO

The gut-brain axis (GBA) refers to the complex interactions between the gut microbiota and the nervous, immune, and endocrine systems, together linking brain and gut functions. Perturbations of the GBA have been reported in people with multiple sclerosis (pwMS), suggesting a possible role in disease pathogenesis and making it a potential therapeutic target. While research in the area is still in its infancy, a number of studies revealed that pwMS are more likely to exhibit altered microbiota, altered levels of short chain fatty acids and secondary bile products, and increased intestinal permeability. However, specific microbes and metabolites identified across studies and cohorts vary greatly. Small clinical and preclinical trials in pwMS and mouse models, in which microbial composition was manipulated through the use of antibiotics, fecal microbiota transplantation, and probiotic supplements, have provided promising outcomes in preventing CNS inflammation. However, results are not always consistent, and large-scale randomized controlled trials are lacking. Herein, we give an overview of how the GBA could contribute to MS pathogenesis, examine the different approaches tested to modulate the GBA, and discuss how they may impact neuroinflammation and demyelination in the CNS.


Assuntos
Microbioma Gastrointestinal , Esclerose Múltipla/terapia , Animais , Autoimunidade , Modelos Animais de Doenças , Disbiose/imunologia , Disbiose/fisiopatologia , Sistema Endócrino/imunologia , Sistema Endócrino/fisiopatologia , Sistema Nervoso Entérico/imunologia , Sistema Nervoso Entérico/microbiologia , Sistema Nervoso Entérico/fisiopatologia , Transplante de Microbiota Fecal , Microbioma Gastrointestinal/efeitos dos fármacos , Microbioma Gastrointestinal/imunologia , Microbioma Gastrointestinal/fisiologia , Humanos , Mucosa Intestinal/imunologia , Mucosa Intestinal/microbiologia , Mucosa Intestinal/fisiopatologia , Modelos Neurológicos , Esclerose Múltipla/etiologia , Esclerose Múltipla/microbiologia , Neuroimunomodulação , Probióticos/uso terapêutico
6.
Toxins (Basel) ; 13(5)2021 05 19.
Artigo em Inglês | MEDLINE | ID: mdl-34069405

RESUMO

Chronic kidney disease (CKD) is a public health concern that affects approximately 10% of the global population. CKD is associated with poor outcomes due to high frequencies of comorbidities such as heart failure and cardiovascular disease. Uremic toxins are compounds that are usually filtered and excreted by the kidneys. With the decline of renal function, uremic toxins are accumulated in the systemic circulation and tissues, which hastens the progression of CKD and concomitant comorbidities. Gut microbial dysbiosis, defined as an imbalance of the gut microbial community, is one of the comorbidities of CKD. Meanwhile, gut dysbiosis plays a pathological role in accelerating CKD progression through the production of further uremic toxins in the gastrointestinal tracts. Therefore, the gut-kidney axis has been attracting attention in recent years as a potential therapeutic target for stopping CKD. Trimethylamine N-oxide (TMAO) generated by gut microbiota is linked to the progression of cardiovascular disease and CKD. Also, advanced glycation endproducts (AGEs) not only promote CKD but also cause gut dysbiosis with disruption of the intestinal barrier. This review summarizes the underlying mechanism for how gut microbial dysbiosis promotes kidney injury and highlights the wide-ranging interventions to counter dysbiosis for CKD patients from the view of uremic toxins such as TMAO and AGEs.


Assuntos
Disbiose/fisiopatologia , Microbioma Gastrointestinal , Insuficiência Renal Crônica/fisiopatologia , Animais , Doenças Cardiovasculares/fisiopatologia , Progressão da Doença , Produtos Finais de Glicação Avançada/metabolismo , Humanos , Metilaminas/metabolismo
7.
Am J Physiol Heart Circ Physiol ; 321(2): H275-H291, 2021 08 01.
Artigo em Inglês | MEDLINE | ID: mdl-34142885

RESUMO

Ethanol consumption represents a significant public health problem, and excessive ethanol intake is a risk factor for cardiovascular disease (CVD), one of the leading causes of death and disability worldwide. The mechanisms underlying the effects of ethanol on the cardiovascular system are complex and not fully comprehended. The gut microbiota and their metabolites are indispensable symbionts essential for health and homeostasis and therefore, have emerged as potential contributors to ethanol-induced cardiovascular system dysfunction. By mechanisms that are not completely understood, the gut microbiota modulates the immune system and activates several signaling pathways that stimulate inflammatory responses, which in turn, contribute to the development and progression of CVD. This review summarizes preclinical and clinical evidence on the effects of ethanol in the gut microbiota and discusses the mechanisms by which ethanol-induced gut dysbiosis leads to the activation of the immune system and cardiovascular dysfunction. The cross talk between ethanol consumption and the gut microbiota and its implications are detailed. In summary, an imbalance in the symbiotic relationship between the host and the commensal microbiota in a holobiont, as seen with ethanol consumption, may contribute to CVD. Therefore, manipulating the gut microbiota, by using antibiotics, probiotics, prebiotics, and fecal microbiota transplantation might prove a valuable opportunity to prevent/mitigate the deleterious effects of ethanol and improve cardiovascular health and risk prevention.


Assuntos
Consumo de Bebidas Alcoólicas/fisiopatologia , Doenças Cardiovasculares/fisiopatologia , Disbiose/fisiopatologia , Microbioma Gastrointestinal , Consumo de Bebidas Alcoólicas/imunologia , Antibacterianos/uso terapêutico , Anti-Infecciosos Locais , Doenças Cardiovasculares/imunologia , Doenças Cardiovasculares/terapia , Disbiose/imunologia , Disbiose/terapia , Etanol , Transplante de Microbiota Fecal , Humanos , Prebióticos , Probióticos/uso terapêutico
8.
Nutrients ; 13(5)2021 May 01.
Artigo em Inglês | MEDLINE | ID: mdl-34062869

RESUMO

Inflammatory bowel disease (IBD) is a chronic inflammatory disease of the gastrointestinal tract. Although the precise etiology of IBD is largely unknown, it is widely thought that diet contributes to the development of IBD. Diet shapes the composition of the gut microbiota, which plays critical roles in intestinal homeostasis. In contrast, intestinal inflammation induces gut dysbiosis and may affect the use of dietary nutrients by host cells and the gut microbiota. The interaction of diet and the gut microbiota is perturbed in patients with IBD. Herein, we review the current knowledge of diet and gut microbiota interaction in intestinal homeostasis. We also discuss alterations of diet and gut microbiota interaction that influence the outcome and the nutritional treatment of IBD. Understanding the complex relationships between diet and the gut microbiota provides crucial insight into the pathogenesis of IBD and advances the development of new therapeutic approaches.


Assuntos
Dieta/efeitos adversos , Ingestão de Alimentos/fisiologia , Microbioma Gastrointestinal/fisiologia , Doenças Inflamatórias Intestinais/microbiologia , Doenças Inflamatórias Intestinais/fisiopatologia , Disbiose/etiologia , Disbiose/microbiologia , Disbiose/fisiopatologia , Homeostase/fisiologia , Humanos , Doenças Inflamatórias Intestinais/etiologia , Intestinos/microbiologia , Intestinos/fisiopatologia
9.
Am Heart J ; 239: 27-37, 2021 09.
Artigo em Inglês | MEDLINE | ID: mdl-33984318

RESUMO

BACKGROUND: Hypertension (HTN) is frequently linked with depression (DEP) in adults with cardiovascular disease (CVD), yet the underlying mechanism and successful management remain elusive. We approached this knowledge gap through the lens that humans are eukaryote-prokaryote "meta-organisms," such that cardiovascular disease dysregulation is a mosaic disorder involving dysbiosis of the gut. We hypothesized that patients diagnosed with hypertension plus depression harbor a unique gut microbial ecology with attending functional genomics engaged with their hosts' gut/brain axis physiology. METHODS: Stool microbiome DNA was analyzed by whole metagenome shotgun sequencing in 54 subjects parsed into cohorts diagnosed with HTN only (N = 18), DEP only (N = 7), DEP plus HTN (DEP-HTN) (N = 8), or reference subjects with neither HTN nor DEP (N = 21). A novel battery of machine-learning multivariate analyses of de-noised data yielded effect sizes and permutational covariance-based dissimilarities that significantly differentiated the cohorts (false discovery rate (FDR)-adjusted P ≤ .05); data clustering within 95% confidence interval). RESULTS: Metagenomic significant differences extricated the four cohorts. Data of the cohort exhibiting DEP-HTN were germane to the interplay of central control of blood pressure concomitant with the neuropathology of depressive disorders. DEP-HTN gut bacterial community ecology was defined by co-occurrence of Eubacterium siraeum, Alistipes obesi, Holdemania filiformis, and Lachnospiraceae bacterium 1.1.57FAA with Streptococcus salivariu. The corresponding microbial functional genomics of DEP-HTN engaged pathways degrading GABA and beneficial short chain fatty acids (SCFA), and are associated with enhanced sodium absorption and inflammasome induction. CONCLUSIONS: These data suggest a new putative endotype of hypertension, which we denote "depressive-hypertension" (DEP-HTN), for which we posit a model that is distinctive from either HTN alone or DEP alone. An "endotype" is a subtype of a heterogeneous pathophysiological mechanism. The DEP-HTN model incorporates a unique signature of microbial taxa and functional genomics with crosstalk that putatively intertwines host pathophysiology involving the gastrointestinal tract with disruptions in central control of blood pressure and mood. The DEP-HTN endotype model engages cardiology with gastroenterology and psychiatry, providing a proof-of-concept foundation to explore future treatments, diagnosis, and prevention of HTN-coupled mood disorders.


Assuntos
Afeto/fisiologia , Biota/genética , Depressão , Disbiose , Microbioma Gastrointestinal , Hipertensão , Adulto , Ciências Biocomportamentais , Depressão/diagnóstico , Depressão/metabolismo , Depressão/fisiopatologia , Disbiose/diagnóstico , Disbiose/fisiopatologia , Disbiose/psicologia , Fezes/microbiologia , Feminino , Microbioma Gastrointestinal/genética , Microbioma Gastrointestinal/fisiologia , Trato Gastrointestinal/microbiologia , Trato Gastrointestinal/fisiopatologia , Humanos , Hipertensão/diagnóstico , Hipertensão/metabolismo , Hipertensão/psicologia , Aprendizado de Máquina , Masculino , Redes e Vias Metabólicas , Metagenoma
10.
Mol Neurobiol ; 58(9): 4477-4486, 2021 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-34033061

RESUMO

The Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), the causative agent of human COVID-19, not only causes flu-like symptoms and gut microbiome complications but a large number of infected individuals also experience a host of neurological symptoms including loss of smell and taste, seizures, difficulty concentrating, decreased alertness, and brain inflammation. Although SARS-CoV-2 infections are not more prevalent in Parkinson's disease patients, a higher mortality rate has been reported not only associated with older age and longer disease duration, but also through several mechanisms, such as interactions with the brain dopaminergic system and through systemic inflammatory responses. Indeed, a number of the neurological symptoms seen in COVID-19 patients, as well as the alterations in the gut microbiome, are also prevalent in patients with Parkinson's disease. Furthermore, biochemical pathways such as oxidative stress, inflammation, and protein aggregation have shared commonalities between Parkinson's disease and COVID-19 disease progression. In this review, we describe and compare the numerous similarities and intersections between neurodegeneration in Parkinson's disease and RNA viral infections, emphasizing the current SARS-CoV-2 global health crisis.


Assuntos
COVID-19/fisiopatologia , Microbioma Gastrointestinal , Doença de Parkinson/fisiopatologia , SARS-CoV-2 , Idoso , COVID-19/complicações , COVID-19/mortalidade , Transtornos Cognitivos/etiologia , Citocinas/fisiologia , Dieta , Progressão da Doença , Disbiose/etiologia , Disbiose/fisiopatologia , Humanos , Inflamação , Metais Pesados/toxicidade , Modelos Neurológicos , Degeneração Neural , Bulbo Olfatório/fisiopatologia , Bulbo Olfatório/virologia , Estresse Oxidativo , Doença de Parkinson/etiologia , Guias de Prática Clínica como Assunto , Agregação Patológica de Proteínas/etiologia , Infecções por Vírus de RNA/metabolismo , Infecções por Vírus de RNA/fisiopatologia , Espécies Reativas de Oxigênio/metabolismo , Transtornos das Sensações/etiologia , alfa-Sinucleína/metabolismo
11.
Med Sci Monit ; 27: e931962, 2021 May 04.
Artigo em Inglês | MEDLINE | ID: mdl-33945520

RESUMO

Trait anxiety is characterized as a constant and often subliminal state that persists during daily life. Interoception is the perception of internal states and sensations, including from the autonomic nervous system. This review aims to develop a predictive model to explain the emergence, manifestations, and maintenance of trait anxiety. The model begins with the assumption that anxiety states arise from active interoceptive inference. The subsequent activation of autonomic responses results from aversive sensory encounters. A cognitive model is proposed for trait anxiety that includes the aversive sensory components from interoception, exteroception, and proprioception. A further component of the hypothesis is that repeated exposure to subliminal anxiety-evoking sensory elements can lead to an overgeneralization of this response to other inputs that are generally non-aversive. Increased uncertainty may result when predicting the sensory environment, resulting in arbitrary interoceptive anxiety responses that may be due to unjustifiable causes. Arbitrary successful or unsuccessful matching of predictions and responses reduces the individual's confidence to maintain the anxiety trait. In this review, the application of the proposed model is illustrated using gut microbial dysbiosis or imbalance of the gut microbiome.


Assuntos
Transtornos de Ansiedade/fisiopatologia , Ansiedade/fisiopatologia , Cognição/fisiologia , Microbioma Gastrointestinal/fisiologia , Interocepção/fisiologia , Disbiose/fisiopatologia , Humanos
12.
Int J Mol Sci ; 22(9)2021 Apr 26.
Artigo em Inglês | MEDLINE | ID: mdl-33926088

RESUMO

Psoriasis is a chronic, immune-mediated inflammatory disease that affects around 125 million people worldwide. Several studies concerning the gut microbiota composition and its role in disease pathogenesis recently demonstrated significant alterations among psoriatic patients. Certain parameters such as Firmicutes/Bacteroidetes ratio or Psoriasis Microbiome Index were developed in order to distinguish between psoriatic and healthy individuals. The "leaky gut syndrome" and bacterial translocation is considered by some authors as a triggering factor for the onset of the disease, as it promotes chronic systemic inflammation. The alterations were also found to resemble those in inflammatory bowel diseases, obesity and certain cardiovascular diseases. Microbiota dysbiosis, depletion in SCFAs production, increased amount of produced TMAO, dysregulation of the pathways affecting the balance between lymphocytes populations seem to be the most significant findings concerning gut physiology in psoriatic patients. The gut microbiota may serve as a potential response-to-treatment biomarker in certain cases of biological treatment. Oral probiotics administration as well as fecal microbial transplantation were most reported in bringing health benefits to psoriatic patients. However, the issue of psoriatic bacterial gut composition, its role and healing potential needs further investigation. Here we reviewed the literature on the current state of the relationship between psoriasis and gut microbiome.


Assuntos
Microbioma Gastrointestinal/fisiologia , Psoríase/metabolismo , Psoríase/microbiologia , Translocação Bacteriana , Bacteroidetes , Doenças Cardiovasculares/microbiologia , Disbiose/fisiopatologia , Firmicutes , Microbioma Gastrointestinal/genética , Humanos , Doenças Inflamatórias Intestinais/microbiologia , Microbiota , Probióticos/uso terapêutico
13.
Nutrients ; 13(2)2021 Feb 13.
Artigo em Inglês | MEDLINE | ID: mdl-33668627

RESUMO

In the past few decades, obesity has reached pandemic proportions. Obesity is among the main risk factors for cardiovascular diseases, since chronic fat accumulation leads to dysfunction in vascular endothelium and to a precocious arterial stiffness. So far, not all the mechanisms linking adipose tissue and vascular reactivity have been explained. Recently, novel findings reported interesting pathological link between endothelial dysfunction with gut hormones and gut microbiota and energy homeostasis. These findings suggest an active role of gut secretome in regulating the mediators of vascular function, such as nitric oxide (NO) and endothelin-1 (ET-1) that need to be further investigated. Moreover, a central role of brain has been suggested as a main player in the regulation of the different factors and hormones beyond these complex mechanisms. The aim of the present review is to discuss the state of the art in this field, by focusing on the processes leading to endothelial dysfunction mediated by obesity and metabolic diseases, such as insulin resistance. The role of perivascular adipose tissue (PVAT), gut hormones, gut microbiota dysbiosis, and the CNS function in controlling satiety have been considered. Further understanding the crosstalk between these complex mechanisms will allow us to better design novel strategies for the prevention of obesity and its complications.


Assuntos
Disbiose/fisiopatologia , Endotélio Vascular/fisiopatologia , Hormônios Gastrointestinais/metabolismo , Microbioma Gastrointestinal/fisiologia , Obesidade/fisiopatologia , Tecido Adiposo/fisiopatologia , Animais , Encéfalo/fisiopatologia , Doenças Cardiovasculares/etiologia , Doenças Cardiovasculares/microbiologia , Doenças Cardiovasculares/fisiopatologia , Disbiose/complicações , Metabolismo Energético/fisiologia , Humanos , Obesidade/complicações , Obesidade/microbiologia , Saciação/fisiologia , Rigidez Vascular/fisiologia
14.
Anal Chim Acta ; 1152: 338267, 2021 Apr 01.
Artigo em Inglês | MEDLINE | ID: mdl-33648648

RESUMO

Although SARS-CoV-2 can invade the intestine, though its effect on digestion and absorption is not fully understood. In the present study, 56 COVID-19 patients and 47 age- and sex-matched healthy subjects were divided into a discovery cohort and a validation cohort. Blood, faeces and clinical information were collected from the patients in the hospital and at discharge. The faecal metabolome was analysed using gas chromatography-mass spectrometry, and Spearman's correlation analyses of clinical features, the serum metabolome, and the faecal micro- and mycobiota were conducted. The results showed that, the faeces of COVID-19 patients were enriched with important nutrients that should be metabolized or absorbed, such as sucrose and 2-palmitoyl-glycerol; diet-related components that cannot be synthesized by humans, such as 1,5-anhydroglucitol and D-pinitol; and harmful metabolites, such as oxalate, were also detected. In contrast, purine metabolites such as deoxyinosine and hypoxanthine, low-water-soluble long-chain fatty alcohols/acids such as behenic acid, compounds rarely occurring in nature such as D-allose and D-arabinose, and microbe-related compounds such as 2,4-di-tert-butylphenol were depleted in the faeces of COVID-19 patients. Moreover, these metabolites significantly correlated with altered serum metabolites such as oxalate and gut microbesincluding Ruminococcaceae, Actinomyces, Sphingomonas and Aspergillus. Although levels of several faecal metabolites, such as sucrose, 1,5-anhydroglucitol and D-pinitol, of discharged patients were not different from those of healthy controls (HCs), those of oxalate and 2-palmitoyl-glycerol did differ. Therefore, alterations in the faecal metabolome of COVID-19 patients may reflect malnutrition and intestinal inflammation and warrant greater attention. The results of present study provide new insights into the pathogenesis and treatment of COVID-19.


Assuntos
COVID-19/fisiopatologia , Disbiose/diagnóstico , Fezes/química , Microbioma Gastrointestinal/fisiologia , Metaboloma/fisiologia , Adulto , Bactérias/metabolismo , Estudos de Coortes , Disbiose/fisiopatologia , Fezes/microbiologia , Feminino , Fungos/metabolismo , Cromatografia Gasosa-Espectrometria de Massas , Humanos , Masculino , Pessoa de Meia-Idade , SARS-CoV-2
15.
Nat Rev Gastroenterol Hepatol ; 18(4): 269-283, 2021 04.
Artigo em Inglês | MEDLINE | ID: mdl-33589829

RESUMO

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has spread to more than 200 countries and regions globally. SARS-CoV-2 is thought to spread mainly through respiratory droplets and close contact. However, reports have shown that a notable proportion of patients with coronavirus disease 2019 (COVID-19) develop gastrointestinal symptoms and nearly half of patients confirmed to have COVID-19 have shown detectable SARS-CoV-2 RNA in their faecal samples. Moreover, SARS-CoV-2 infection reportedly alters intestinal microbiota, which correlated with the expression of inflammatory factors. Furthermore, multiple in vitro and in vivo animal studies have provided direct evidence of intestinal infection by SARS-CoV-2. These lines of evidence highlight the nature of SARS-CoV-2 gastrointestinal infection and its potential faecal-oral transmission. Here, we summarize the current findings on the gastrointestinal manifestations of COVID-19 and its possible mechanisms. We also discuss how SARS-CoV-2 gastrointestinal infection might occur and the current evidence and future studies needed to establish the occurrence of faecal-oral transmission.


Assuntos
COVID-19/fisiopatologia , Diarreia/fisiopatologia , Disbiose/fisiopatologia , Gastroenterite/fisiopatologia , Microbioma Gastrointestinal , Náusea/fisiopatologia , Vômito/fisiopatologia , Dor Abdominal/fisiopatologia , Enzima de Conversão de Angiotensina 2/metabolismo , Animais , Anorexia/fisiopatologia , COVID-19/transmissão , Linhagem Celular , Colo/metabolismo , Citocinas/metabolismo , Modelos Animais de Doenças , Fezes/química , Gastroenterite/virologia , Humanos , Mucosa Intestinal/metabolismo , Intestino Delgado/metabolismo , Complexo Antígeno L1 Leucocitário/metabolismo , Organoides , RNA Viral , Receptores de Coronavírus/metabolismo , SARS-CoV-2/metabolismo , Serina Endopeptidases/metabolismo , Carga Viral , Eliminação de Partículas Virais
16.
Neurogastroenterol Motil ; 33(3): e14104, 2021 03.
Artigo em Inglês | MEDLINE | ID: mdl-33591607

RESUMO

BACKGROUND: Coronavirus disease 2019 (COVID-19) is associated with gastrointestinal and hepatic manifestation in up to one fifth of patients. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the etiologic agent of COVID-19, infects gastrointestinal epithelial cells expressing angiotensin-converting enzyme 2 (ACE2) receptors triggering a cascade of events leading to mucosal and systemic inflammation. Symptomatic patients display changes in gut microbiota composition and function which may contribute to intestinal barrier dysfunction and immune activation. Evidence suggests that SARS-CoV-2 infection and related mucosal inflammation impact on the function of the enteric nervous system and the activation of sensory fibers conveying information to the central nervous system, which, may at least in part, contribute symptom generation such as vomiting and diarrhea described in COVID-19. Liver and pancreas dysfunctions have also been described as non-respiratory complications of COVID-19 and add further emphasis to the common view of SARS-CoV-2 infection as a systemic disease with multiorgan involvement. PURPOSE: The aim of this review was to highlight the current knowledge on the pathophysiology of gastrointestinal SARS-CoV-2 infection, including the crosstalk with the gut microbiota, the fecal-oral route of virus transmission, and the potential interaction of the virus with the enteric nervous system. We also review the current available data on gastrointestinal and liver manifestations, management, and outcomes of patients with COVID-19.


Assuntos
COVID-19/complicações , COVID-19/fisiopatologia , Gastroenteropatias/etiologia , Gastroenteropatias/fisiopatologia , Microbioma Gastrointestinal/fisiologia , Trato Gastrointestinal/fisiopatologia , Animais , Diarreia/etiologia , Diarreia/fisiopatologia , Diarreia/virologia , Disbiose/etiologia , Disbiose/fisiopatologia , Disbiose/virologia , Sistema Nervoso Entérico/fisiopatologia , Sistema Nervoso Entérico/virologia , Gastroenteropatias/virologia , Trato Gastrointestinal/virologia , Humanos , Hepatopatias/etiologia , Hepatopatias/fisiopatologia , Hepatopatias/virologia , Pancreatopatias/etiologia , Pancreatopatias/fisiopatologia , Pancreatopatias/virologia
17.
Sci Rep ; 11(1): 741, 2021 01 12.
Artigo em Inglês | MEDLINE | ID: mdl-33436882

RESUMO

Human activities interfere with wild animals and lead to the loss of many animal populations. Therefore, efforts have been made to understand how wildlife can rebound from anthropogenic disturbances. An essential mechanism to adapt to environmental and social changes is the fluctuations in the host gut microbiome. Here we give a comprehensive description of anthropogenically induced microbiome alterations in Asian elephants (n = 30). We detected gut microbial changes due to overseas translocation, captivity and deworming. We found that microbes belonging to Planococcaceae had the highest contribution in the microbiome alterations after translocation, while Clostridiaceae, Spirochaetaceae and Bacteroidia were the most affected after captivity. However, deworming significantly changed the abundance of Flavobacteriaceae, Sphingobacteriaceae, Xanthomonadaceae, Weeksellaceae and Burkholderiaceae. These findings may provide fundamental ideas to help guide the preservation tactics and probiotic replacement therapies of a dysbiosed gut microbiome in Asian elephants. More generally, these results show the severity of anthropogenic activities at the level of gut microbiome, altering the adaptation processes to new environments and the subsequent capability to maintain normal physiological processes in animals.


Assuntos
Adaptação Fisiológica , Disbiose/fisiopatologia , Ecossistema , Elefantes/microbiologia , Monitoramento Ambiental/métodos , Microbioma Gastrointestinal , Animais , Ásia , Disbiose/microbiologia , Feminino , Masculino
18.
J Drugs Dermatol ; 20(1): 62-69, 2021 01 01.
Artigo em Inglês | MEDLINE | ID: mdl-33400410

RESUMO

Although the relationship between psychosocial stress and skin health is commonly invoked in both the scientific and popular literature, its underlying mechanisms are still not well understood. In this review, we provide a comprehensive update on the pathophysiology of stress and its clinical impact on skin homeostasis. The recent characterization of a bidirectional HPA stress axis in the skin has illuminated peripheral stress pathways, with effects spanning inflammation, atopy, barrier function, dermal thinning, wound healing, and melanogenesis. Additionally, new research into the cutaneous microbiome suggests the development of stress-induced dysbiosis through the “gut-brain-skin” axis. These new findings help contextualize how lifestyle factors such as diet, personal care practices, and sleep patterns may mediate and sometimes amplify the cutaneous impacts of psychological stress. We aim to clarify these clinically important relationships and highlight areas of future study that have widespread academic, clinical, and commercial implications. J Drugs Dermatol. 2021;20(1):62-29. doi:10.36849/JDD.5608.


Assuntos
Disbiose/fisiopatologia , Sistema Hipotálamo-Hipofisário/fisiologia , Fenômenos Fisiológicos da Pele , Estresse Psicológico/complicações , Disbiose/etiologia , Disbiose/microbiologia , Microbioma Gastrointestinal/fisiologia , Humanos , Estilo de Vida , Sono/fisiologia , Estresse Psicológico/fisiopatologia
19.
J Appl Microbiol ; 130(1): 14-24, 2021 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-32692438

RESUMO

The gut microbiome is well recognized to have a pivotal role in regulation of the health and behaviour of the host, affecting digestion, metabolism, immunity, and has been linked to changes in bones, muscles and the brain, to name a few. However, the impact of microgravity environment on gut bacteria is not well understood. In space environments, astronauts face several health issues including stress, high iron diet, radiation and being in a closed system during extended space missions. Herein, we discuss the role of gut bacteria in the space environment, in relation to factors such as microgravity, radiation and diet. Gut bacteria may exact their effects by synthesis of molecules, their absorption, and through physiological effects on the host. Moreover we deliberate the role of these challenges in the dysbiosis of the human microbiota and possible dysregulation of the immune system.


Assuntos
Meio Ambiente Extraterreno , Microbioma Gastrointestinal/fisiologia , Dieta/efeitos adversos , Disbiose/fisiopatologia , Humanos , Sistema Imunitário/fisiologia , Sistema Imunitário/efeitos da radiação , Radiação , Voo Espacial , Estresse Fisiológico/fisiologia , Estresse Fisiológico/efeitos da radiação , Ausência de Peso/efeitos adversos
20.
Gastroenterology ; 160(2): 483-494, 2021 01.
Artigo em Inglês | MEDLINE | ID: mdl-33253682

RESUMO

Use of microbiome-based biomarkers in diagnosis, prognosis, risk profiling, and precision therapy requires definition of a healthy microbiome in different populations. To determine features of the intestinal microbiota associated with health, however, we need improved microbiome profiling technologies, with strain-level resolution. We must also learn more about how the microbiome varies among apparently healthy people, how it changes with age, and the effects of diet, medications, ethnicity, geography, and lifestyle. Furthermore, many intestinal microbes, including viruses, phage, fungi, and archaea, have not been characterized, and little is known about their contributions to health and disease.Whether a healthy microbiome can be defined is an important and seemingly simple question, but with a complex answer in continual need of refinement.


Assuntos
Microbioma Gastrointestinal , Interações entre Hospedeiro e Microrganismos/fisiologia , Disbiose/microbiologia , Disbiose/fisiopatologia , Meio Ambiente , Microbioma Gastrointestinal/fisiologia , Saúde/normas , Nível de Saúde , Humanos , Estilo de Vida , Microbiota/fisiologia , Padrões de Referência , Risco
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