Omics for deciphering oral microecology / 国际口腔科学杂志·英文版

The human oral microbiome harbors one of the most diverse microbial communities in the human body, playing critical roles in oral and systemic health. Recent technological innovations are propelling the characterization and manipulation of oral microbiota. High-throughput sequencing enables comprehensive taxonomic and functional profiling of oral microbiomes. New long-read platforms improve genome assembly from complex samples. Single-cell genomics provides insights into uncultured taxa. Advanced imaging modalities including fluorescence, mass spectrometry, and Raman spectroscopy have enabled the visualization of the spatial organization and interactions of oral microbes with increasing resolution. Fluorescence techniques link phylogenetic identity with localization. Mass spectrometry imaging reveals metabolic niches and activities while Raman spectroscopy generates rapid biomolecular fingerprints for classification. Culturomics facilitates the isolation and cultivation of novel fastidious oral taxa using high-throughput approaches. Ongoing integration of these technologies holds the promise of transforming our understanding of oral microbiome assembly, gene expression, metabolites, microenvironments, virulence mechanisms, and microbe-host interfaces in the context of health and disease. However, significant knowledge gaps persist regarding community origins, developmental trajectories, homeostasis versus dysbiosis triggers, functional biomarkers, and strategies to deliberately reshape the oral microbiome for therapeutic benefit. The convergence of sequencing, imaging, cultureomics, synthetic systems, and biomimetic models will provide unprecedented insights into the oral microbiome and offer opportunities to predict, prevent, diagnose, and treat associated oral diseases.

The impact of intestinal microbiota imbalance on the development of obesity / O impacto do desequilíbrio da microbiota intestinal no desenvolvimento da obesidade

Objective: review current databases to identify the impacts of intestinal dysbiosis on obesity, as well as serve as a pillar for carrying out preventive, diagnostic and therapeutic measures. Methodology: this is an integrative review carried out from the collection of data obtained from the SciELO, PubMed, VHL, and LILACS platforms using the descriptors "dysbiosis", "obesity" and "gastrointestinal microbiome"; Inclusion criteria were: articles published in the last five years (from 2017 to 2022), original articles, meta-analyses, and observational studies (clinical trials and cohort study) and written in Portuguese, English, or Spanish. Results: Western diet and use of sweeteners cause anthropometric changes, blood pressure, glucose intolerance, among others, in addition to leading to the prevalence of deleterious bacteria in the body, culminating in obesity and diabetes mellitus; on the other hand, a diet rich in fiber and administration of probiotics can generate beneficial changes in the diversity of the intestinal flora, in addition to combating the inflammatory state generated by obesity (AU).

Objetivo: revisar as bases de dados atuais para identificar os impactos da disbiose intestinal na obesidade, bem como servir de pilar para realização de medidas preventivas, diagnósticas e terapêuticas. Metodologia: trata-se de revisão integrativa realizada a partir de coleta de dados obtidos nas plataformas SciELO, PuBMed, BVS e LILACS usando os descritores "dysbiosis", "obesity" and "gastrointestinal microbiome"; os critérios de inclusão foram: artigos publicados nos últimos cinco anos (de 2017 a 2022), artigos originais, metanálises e estudos observacionais (ensaios clínicos e estudo de coorte) e escritos em português, inglês ou espanhol. Resultados: dieta ocidental e uso de adoçante provocam alterações antropométricas, de pressão arterial, intolerância à glicose, entre outras, além de levar à prevalência de bactérias deletérias ao organismo, culminando em obesidade e diabetes mellitus; em contrapartida, dieta rica em fibras e administração de probióticos podem gerar mudanças benéficas na diversidade da flora intestinal, ademais combatem o estado inflamatório gerado pela obesidade (AU).

Gut dysbiosis, inflammation and type 2 diabetes in mice using synthetic gut microbiota from diabetic humans / Disbiose intestinal, inflamação e diabetes tipo 2 em camundongos usando microbiota intestinal sintética de humanos diabéticos

The study was aimed to assess impact of high fat diet (HFD) and synthetic human gut microbiota (GM) combined with HFD and chow diet (CD) in inducing type-2 diabetes (T2D) using mice model. To our knowledge, this is the first study using selected human GM transplantation via culture based method coupled dietary modulation in mice for in vivo establishment of inflammation leading to T2D and gut dysbiosis. Twenty bacteria (T2D1-T2D20) from stool samples of confirmed T2D subjects were found to be morphologically different and subjected to purification on different media both aerobically and anerobically, which revealed seven bacteria more common among 20 isolates on the basis of biochemical characterization. On the basis of 16S rRNA gene sequencing, these seven isolates were identified as Bacteroides stercoris (MT152636), Lactobacillus acidophilus (MT152637), Lactobacillus salivarius (MT152638), Ruminococcus bromii (MT152639), Klebsiella aerogenes (MT152640), Bacteroides fragilis (MT152909), Clostridium botulinum (MT152910). The seven isolates were subsequently used as synthetic gut microbiome (GM) for their role in inducing T2D in mice. Inbred strains of albino mice were divided into four groups and were fed with CD, HFD, GM+HFD and GM+CD. Mice receiving HFD and GM+modified diet (CD/HFD) showed highly significant (P<0.05) increase in weight and blood glucose concentration as well as elevated level of inflammatory cytokines (TNF-α, IL-6, and MCP-1) compared to mice receiving CD only. The 16S rRNA gene sequencing of 11 fecal bacteria obtained from three randomly selected animals from each group revealed gut dysbiosis in animals receiving GM. Bacterial strains including Bacteroides gallinarum (MT152630), Ruminococcus bromii (MT152631), Lactobacillus acidophilus (MT152632), Parabacteroides gordonii (MT152633), Prevotella copri (MT152634) and Lactobacillus gasseri (MT152635) were isolated from mice [...].

O estudo teve como objetivo avaliar o impacto da dieta rica em gordura (HFD) e da microbiota intestinal humana sintética (GM) combinada com HFD e dieta alimentar (CD) na indução de diabetes tipo 2 (T2D) usando modelo de camundongos. Para nosso conhecimento, este é o primeiro estudo usando transplante de GM humano selecionado através do método baseado em cultura acoplada à modulação dietética em camundongos para o estabelecimento in vivo de inflamação que leva a T2D e disbiose intestinal. Vinte bactérias (T2D1-T2D20) de amostras de fezes de indivíduos T2D confirmados verificaram ser morfologicamente diferentes e foram submetidas à purificação em meios diferentes aerobicamente e anaerobicamente, o que revelou sete bactérias mais comuns entre 20 isolados com base na caracterização bioquímica. Com base no sequenciamento do gene 16S rRNA, esses sete isolados foram identificados como Bacteroides stercoris (MT152636), Lactobacillus acidophilus (MT152637), Lactobacillus salivarius (MT152638), Ruminococcus bromii (MT152639), Klebsiella aerogenides (MT152640), Bacteroides fragilis (MT152909), Clostridium botulinum (MT152910). Esses sete isolados foram, posteriormente, usados como microbioma intestinal sintético (GM) por seu papel na indução de T2D em camundongos. Linhagens consanguíneas de camundongos albinos foram divididas em quatro grupos e foram alimentadas com CD, HFD, GM + HFD e GM + CD. Camundongos que receberam a dieta modificada com HFD e GM + (CD / HFD) mostraram um aumento altamente significativo (P < 0,05) no peso e na concentração de glicose no sangue, bem como um nível elevado de citocinas inflamatórias (TNF-α, IL-6 e MCP-1) em comparação com os ratos que receberam apenas CD. O sequenciamento do gene 16S rRNA de 11 bactérias fecais obtidas de três animais selecionados aleatoriamente de cada grupo revelou disbiose intestinal em animais que receberam GM. Cepas bacterianas, incluindo Bacteroides gallinarum (MT152630), Ruminococcus [...].

Gut microbial dysbiosis under space environment: a review / 生物工程学报

Unique factors in the space environment can cause dysbiosis of astronauts' gut microbiota and its metabolites, which may exert systematic physiological effects on human body. Recent progress regarding the effect of space flight/simulated space environment (SF/SPE) on the composition of gut microbiota and its metabolites was reviewed in this paper. SF/SPE may cause the increase of invasive pathogenic bacteria and the decrease of beneficial bacteria, aggravating intestinal inflammation and increasing intestinal permeability. SF/SPE may also cause the decrease of beneficial metabolites or the increase of harmful metabolites of gut microbiota, leading to metabolism disorder in vivo, or inducing damage of other systems, thus not beneficial to the health and working efficiency of astronauts. Summarizing the effects of SF/SPE on gut microbiota may provide scientific basis for further researches in this field and the on-orbit health protection of astronauts.

Metformin may be a viable adjunctive therapeutic option to potentially enhance immune reconstitution in HIV-positive immunological non-responders / 中华医学杂志(英文版)

Incomplete immune reconstitution remains a global challenge for human immunodeficiency virus (HIV) treatment in the present era of potent antiretroviral therapy (ART), especially for those individuals referred to as immunological non-responders (INRs), who exhibit dramatically low CD4 + T-cell counts despite the use of effective antiretroviral therapy, with long-term inhibition of viral replication. In this review, we provide a critical overview of the concept of ART-treated HIV-positive immunological non-response, and also explain the known mechanisms which could potentially account for the emergence of immunological non-response in some HIV-infected individuals treated with appropriate and effective ART. We found that immune cell exhaustion, combined with chronic inflammation and the HIV-associated dysbiosis syndrome, may represent strategic aspects of the immune response that may be fundamental to incomplete immune recovery. Interestingly, we noted from the literature that metformin exhibits properties and characteristics that may potentially be useful to specifically target immune cell exhaustion, chronic inflammation, and HIV-associated gut dysbiosis syndrome, mechanisms which are now recognized for their critically important complicity in HIV disease-related incomplete immune recovery. In light of evidence discussed in this review, it can be seen that metformin may be of particularly favorable use if utilized as adjunctive treatment in INRs to potentially enhance immune reconstitution. The approach described herein may represent a promising area of therapeutic intervention, aiding in significantly reducing the risk of HIV disease progression and mortality in a particularly vulnerable subgroup of HIV-positive individuals.

Systemic antibiotics increase microbiota pathogenicity and oral bone loss / 国际口腔科学杂志·英文版

Periodontitis is the most widespread oral disease and is closely related to the oral microbiota. The oral microbiota is adversely affected by some pharmacologic treatments. Systemic antibiotics are widely used for infectious diseases but can lead to gut dysbiosis, causing negative effects on the human body. Whether systemic antibiotic-induced gut dysbiosis can affect the oral microbiota or even periodontitis has not yet been addressed. In this research, mice were exposed to drinking water containing a cocktail of four antibiotics to explore how systemic antibiotics affect microbiota pathogenicity and oral bone loss. The results demonstrated, for the first time, that gut dysbiosis caused by long-term use of antibiotics can disturb the oral microbiota and aggravate periodontitis. Moreover, the expression of cytokines related to Th17 was increased while transcription factors and cytokines related to Treg were decreased in the periodontal tissue. Fecal microbiota transplantation with normal mice feces restored the gut microbiota and barrier, decreased the pathogenicity of the oral microbiota, reversed the Th17/Treg imbalance in periodontal tissue, and alleviated alveolar bone loss. This study highlights the potential adverse effects of long-term systemic antibiotics-induced gut dysbiosis on the oral microbiota and periodontitis. A Th17/Treg imbalance might be related to this relationship. Importantly, these results reveal that the periodontal condition of patients should be assessed regularly when using systemic antibiotics in clinical practice.

Rice bran oil supplementation protects swine weanlings against diarrhea and lipopolysaccharide challenge / 浙江大学学报（英文版）（B辑：生物医学和生物技术）

Early weaned piglets suffer from oxidative stress and enteral infection, which usually results in gut microbial dysbiosis, serve diarrhea, and even death. Rice bran oil (RBO), a polyphenol-enriched by-product of rice processing, has been shown to have antioxidant and anti-inflammatory properties both in vivo and in vitro. Here, we ascertained the proper RBO supplementation level, and subsequently determined its effects on lipopolysaccharide (LPS)-induced intestinal dysfunction in weaned piglets. A total of 168 piglets were randomly allocated into four groups of seven replicates (42 piglets each group, (21±1) d of age, body weight (7.60±0.04) kg, and half males and half females) and were given basal diet (Ctrl) or basal diet supplemented with 0.01% (mass fraction) RBO (RBO1), 0.02% RBO (RBO2), or 0.03% RBO (RBO3) for 21 d. Then, seven piglets from the Ctrl and the RBO were treated with LPS (100 μg/kg body weight (BW)) as LPS group and RBO+LPS group, respectively. Meanwhile, seven piglets from the Ctrl were treated with the saline vehicle (Ctrl group). Four hours later, all treated piglets were sacrificed for taking samples of plasma, jejunum tissues, and feces. The results showed that 0.02% was the optimal dose of dietary RBO supplementation based on diarrhea, average daily gain, and average daily feed intake indices in early weaning piglets. Furthermore, RBO protected piglets against LPS-induced jejunal epithelium damage, which was indicated by the increases in villus height, villus height/crypt depth ratio, and Claudin-1 levels, as well as a decreased level of jejunal epithelium apoptosis. RBO also improved the antioxidant ability of LPS-challenged piglets, which was indicated by the elevated concentrations of catalase and superoxide dismutase, and increased total antioxidant capacity, as well as the decreased concentrations of diamine oxidase and malondialdehyde in plasma. Meanwhile, RBO improved the immune function of LPS-challenged weaned piglets, which was indicated by elevated immunoglobulin A (IgA), IgM, β‍‍-defensin-1, and lysozyme levels in the plasma. In addition, RBO supplementation improved the LPS challenge-induced dysbiosis of gut microbiota. Particularly, the indices of antioxidant capacity, intestinal damage, and immunity were significantly associated with the RBO-regulated gut microbiota. These findings suggested that 0.02% RBO is a suitable dose to protect against LPS-induced intestinal damage, oxidative stress, and jejunal microbiota dysbiosis in early weaned piglets.

Alteración de la microbiota intestinal y su relación con enfermedades gastrointestinales y hepatobiliares / Disruption of the intestinal microbiota and its relationship with gastrointestinal and hepatobiliary diseases

La interrupción de la simbiosis que existe entre el cuerpo humano y su microbioma puede resultar en una disbiosis, un desequilibrio en la interacción huésped-microbiota, que puede asociarse al desarrollo de diversas enfermedades como el síndrome de intestino irritable, hígado graso no alco-hólico, enfermedad hepática alcohólica y cirrosis, entre otras. En ciertas condiciones patológicas y por múltiples factores de riesgo, la capacidad de autorregulación del intestino se puede alterar, contribuyendo al incremento de la permeabilidad con inflamación intestinal crónica. El diagnóstico y el tratamiento, así como la relación entre la permeabilidad intestinal, la disbiosis y las patologías gastrointestinales y hepatobiliares, todavía no tienen estudios clínicos validados o con el soporte científico adecuado, por lo que se realiza una revisión de la literatura con la finalidad de aportar conceptos que puedan orientar con respecto a la importancia del estudio del microbioma humano en estas enfermedades.

Disruption of the symbiosis that exists between the human body and its microbiome can result in dys-biosis, an imbalance in the host-microbiota interaction, which may be associated with the develop-ment of various diseases such as irritable bowel syndrome, non-alcoholic fatty liver disease, alcoholic liver disease and cirrhosis, among others. In certain pathological conditions and due to multiple risk factors, the self-regulating capacity of the intestine may be lost, contributing to increased permeability with chronic intestinal inflammation. Its diagnosis and treatment as well as the relationship between intestinal permeability, dysbiosis and gastrointestinal and hepatobiliary pathologies have not been validated in clinical studies or have adequate scientific support, so a review of the literature is carried out in order to provide concepts that can guide with respect to the importance of the study of the human microbiome in these diseases

Gut dysbiosis, inflammation and type 2 diabetes in mice using synthetic gut microbiota from diabetic humans / Disbiose intestinal, inflamação e diabetes tipo 2 em camundongos usando microbiota intestinal sintética de humanos diabéticos

Abstract The study was aimed to assess impact of high fat diet (HFD) and synthetic human gut microbiota (GM) combined with HFD and chow diet (CD) in inducing type-2 diabetes (T2D) using mice model. To our knowledge, this is the first study using selected human GM transplantation via culture based method coupled dietary modulation in mice for in vivo establishment of inflammation leading to T2D and gut dysbiosis. Twenty bacteria (T2D1-T2D20) from stool samples of confirmed T2D subjects were found to be morphologically different and subjected to purification on different media both aerobically and anerobically, which revealed seven bacteria more common among 20 isolates on the basis of biochemical characterization. On the basis of 16S rRNA gene sequencing, these seven isolates were identified as Bacteroides stercoris (MT152636), Lactobacillus acidophilus (MT152637), Lactobacillus salivarius (MT152638), Ruminococcus bromii (MT152639), Klebsiella aerogenes (MT152640), Bacteroides fragilis (MT152909), Clostridium botulinum (MT152910). The seven isolates were subsequently used as synthetic gut microbiome (GM) for their role in inducing T2D in mice. Inbred strains of albino mice were divided into four groups and were fed with CD, HFD, GM+HFD and GM+CD. Mice receiving HFD and GM+modified diet (CD/HFD) showed highly significant (P<0.05) increase in weight and blood glucose concentration as well as elevated level of inflammatory cytokines (TNF-α, IL-6, and MCP-1) compared to mice receiving CD only. The 16S rRNA gene sequencing of 11 fecal bacteria obtained from three randomly selected animals from each group revealed gut dysbiosis in animals receiving GM. Bacterial strains including Bacteroides gallinarum (MT152630), Ruminococcus bromii (MT152631), Lactobacillus acidophilus (MT152632), Parabacteroides gordonii (MT152633), Prevotella copri (MT152634) and Lactobacillus gasseri (MT152635) were isolated from mice treated with GM+modified diet (HFD/CD) compared to strains Akkermansia muciniphila (MT152625), Bacteriodes sp. (MT152626), Bacteroides faecis (MT152627), Bacteroides vulgatus (MT152628), Lactobacillus plantarum (MT152629) which were isolated from mice receiving CD/HFD. In conclusion, these findings suggest that constitution of GM and diet plays significant role in inflammation leading to onset or/and possibly progression of T2D. .

Resumo O estudo teve como objetivo avaliar o impacto da dieta rica em gordura (HFD) e da microbiota intestinal humana sintética (GM) combinada com HFD e dieta alimentar (CD) na indução de diabetes tipo 2 (T2D) usando modelo de camundongos. Para nosso conhecimento, este é o primeiro estudo usando transplante de GM humano selecionado através do método baseado em cultura acoplada à modulação dietética em camundongos para o estabelecimento in vivo de inflamação que leva a T2D e disbiose intestinal. Vinte bactérias (T2D1-T2D20) de amostras de fezes de indivíduos T2D confirmados verificaram ser morfologicamente diferentes e foram submetidas à purificação em meios diferentes aerobicamente e anaerobicamente, o que revelou sete bactérias mais comuns entre 20 isolados com base na caracterização bioquímica. Com base no sequenciamento do gene 16S rRNA, esses sete isolados foram identificados como Bacteroides stercoris (MT152636), Lactobacillus acidophilus (MT152637), Lactobacillus salivarius (MT152638), Ruminococcus bromii (MT152639), Klebsiella aerogenides (MT152640), Bacteroides fragilis (MT152909), Clostridium botulinum (MT152910). Esses sete isolados foram, posteriormente, usados ​​como microbioma intestinal sintético (GM) por seu papel na indução de T2D em camundongos. Linhagens consanguíneas de camundongos albinos foram divididas em quatro grupos e foram alimentadas com CD, HFD, GM + HFD e GM + CD. Camundongos que receberam a dieta modificada com HFD e GM + (CD / HFD) mostraram um aumento altamente significativo (P < 0,05) no peso e na concentração de glicose no sangue, bem como um nível elevado de citocinas inflamatórias (TNF-α, IL-6 e MCP-1) em comparação com os ratos que receberam apenas CD. O sequenciamento do gene 16S rRNA de 11 bactérias fecais obtidas de três animais selecionados aleatoriamente de cada grupo revelou disbiose intestinal em animais que receberam GM. Cepas bacterianas, incluindo Bacteroides gallinarum (MT152630), Ruminococcus bromii (MT152631), Lactobacillus acidophilus (MT152632), Parabacteroides gordonii (MT152633), Prevotella copri (MT152634) e Lactobacillus Gasseri (MT152635D), foram tratadas com dieta modificada / CD) em comparação com as linhagens Akkermansia muciniphila (MT152625), Bacteriodes sp. (MT152626), Bacteroides faecis (MT152627), Bacteroides vulgatus (MT152628), Lactobacillus plantarum (MT152629), que foram isoladas de camundongos recebendo CD / HFD. Em conclusão, esses resultados sugerem que a constituição de GM e dieta desempenham papel significativo na inflamação levando ao início ou/e possivelmente à progressão de T2D.

Consumo de Castanha-do-Brasil reduz o N-óxido de trimetilamina (TMAO) e a inflamação em um paciente com síndrome cardiorrenal: uma comunicação breve / Brazil nut consumption reduces trimethylamine-n-oxide (TMAO) and inflammation in a patient with cardiorenal syndrome: a brief communication

Introdução: A disbiose intestinal é uma característica comum na síndrome cardiorrenal e está associada ao aumento de toxinas urêmicas, como o N-óxido de trimetilamina (TMAO), que estão envolvidas com a inflamação e mortalidade cardiovascular. A castanha-do-Brasil (semente típica brasileira) possui propriedades anti-inflamatórias e antioxidantes, mas não há evidências dos seus efeitos na modulação da microbiota intestinal e redução de toxinas urêmicas. Objetivo: Avaliar o impacto do consumo de castanha-do-Brasil nos níveis de TMAO e marcadores de inflamação em um paciente com síndrome cardiorrenal. Métodos: Um paciente com doença arterial coronariana (66 anos e IMC, 26 kg/m2), estágio 3 da DRC (TFGe 36 mL/min), recebeu uma castanha-do-Brasil por dia durante três meses. Resultados: Os níveis plasmáticos de TMAO e a expressão de mRNA de NF-κB foram reduzidos e a atividade da glutationa peroxidase (GPx) aumentou após esta intervenção. Conclusão: A prescrição de castanha-do-Brasil pode ser uma estratégia promissora para mitigar as complicações relacionadas à síndrome cardiorrenal. Este caso apoia o conceito de "alimento como remédio" visando o fenótipo urêmico na síndrome cardiorrenal.

Introduction: Gut dysbiosis is a common feature in cardiorenal syndrome, and it is linked to increased uremic toxins, like trimethylamine-n-oxide (TMAO), which are involved with inflammation and cardiovascular mortality. Brazil nut (typical Brazilian seed) has anti-inflammatory and antioxidant properties, but there is no evidence of the effects of gut microbiota modulation and reduction of uremic toxins. Objective: To assess the impact of Brazil nut consumption on TMAO levels and inflammation markers in a patient with cardiorenal syndrome. Methods: Acoronary artery disease patient(66 years and BMI, 26 kg/m2),stage-3 of CKD (eGFR 36 mL/min), receivedone Brazil nut per day for three months. Results: TMAO plasma levels and NF-κB mRNA expression were reduced, and glutathione peroxidase (GPx) activity increased after this intervention. Conclusion: Brazil nut prescription may be a promising strategy to mitigate complications related tothe cardiorenal syndrome. This case supports the concept of "Food as medicine" targeting the uremic phenotype in cardiorenal syndrome.

In sickness and in health: the intestinal microbiome of dogs / Na saúde e na doença: os efeitos do microbioma intestinal no cão

Studies on the interactions between the intestinal microbiome and its host have strengthened in the last decade. However, publications on this topic in dogs still need to be made available, reinforcing the need for new studies and literary data for consultation. Given this, this review aims to describe the intestinal microbiome and its interactions with the canine host, which can contribute to both health and morbid conditions in these animals. The definition of microbiome encompasses the collective genome of all microorganisms that live in a defined habitat (intestine). It is known that the dog's intestinal microbiota is varied, composed of bacteria, archaea, viruses, fungi, and protozoa. Under normal conditions, there is commensalism between some of these microorganisms and the host, which promotes critical physiological relationships and interactions that contribute to homeostasis and the consequent health of the animal. With this in mind, it is expected that the disturbances associated with the microbiome will result in imbalances in this commensal relationship and thus precipitate the development of diseases and aggravation of other diseases, thus characterizing intestinal dysbiosis.(AU)

Os estudos sobre as interações entre o microbioma intestinal e o seu hospedeiro ganharam força na última década. Entretanto, as publicações acerca de tal temática em cães ainda são escassas, o que reforça a necessidade de novos estudos e dados literários para consultas. Frente a isso, o objetivo da presente revisão é descrever sobre o microbioma intestinal e suas interações e principais efeitos no cão, os quais podem contribuir tanto para a higidez quanto para quadros mórbidos desses animais. A definição de microbioma engloba o genoma coletivo de todos os microrganismos que vivem em habitat definido (intestino). É sabido que a microbiota intestinal do cão é muito variada, sendo composta por bactérias, arqueas, vírus, fungos e protozoários. Em condições normais, há o comensalismo entre alguns desses microrganismos e o hospedeiro, o que promove importantes relações e interações fisiológicas que contribuem sobremaneira para a homeostasia e consequente saúde do animal. Ciente disso, é de se esperar que os distúrbios associados ao microbioma resultarão em desequilíbrios nessa relação comensal e, assim, precipitar o desenvolvimento de doenças e/ou agravamento de outras moléstias, caracterizando, assim, a disbiose intestinal.(AU)

A relação do transtorno do espectro autista e a disbiose intestinal: uma revisão integrativa / The relationship between autism spectrum disorder and intestinal dysbiosis: an integrative review

Objetivos: evidenciar as relações e a existência do agravamento do Transtorno do Espectro Autista devido à disbiose intestinal. Métodos: revisão integrativa realizada segundo a pergunta norteadora: Existe comprovação científica entre a relação do TEA e disbiose intestinal que favoreça a melhora na prática clínica e indicações de possíveis respostas? Buscou-se por artigos publicados entre janeiro de 2016 e janeiro de 2021, nas bases de dados: PubMed, SciELO, LILACS, GOOGLE ACADÊMICO. Foram utilizados os descritores (DeCS): "Transtorno do Espectro Autista"; "Microbiota gastrointestinal"; "Disbiose", associados pelo operador booleano "E". Foram incluidos artigos de revisões bibliográficas, completos, originais, limitados aos idiomas inglês e português brasileiro, publicados nos últimos cinco anos, e que, após leitura do resumo, estivessem dentro do escopo da revisão. Resultados: Foram identificados 52 manuscritos e, após aplicação dos critérios de inclusão e exclusão, foram considerados 11 artigos que evidenciam o agravamento do TEA por fatores intrínsecos à microbiota intestinal. Conclusão: existe importante influência causal do eixo bidirecional cérebro-intestino-microbiota na etiologia e exacerbaçao das manifestações clínicas do Transtorno do Espectro Autista devido à disbiose intestinal e aos fatores gastrointestinais de origem idiopática.

Objectives: to highlight the relationships and the existence of Autistic Spectrum Disorder aggravation due to intestinal dysbiosis. Methods: integrative review conducted according to the guiding question: Is there scientific evidence of the relationship between ASD and intestinal dysbiosis that favors improvement in clinical practice and indications of possible answers? We searched for articles published between January 2016 and January 2021 in databases: PubMed, SciELO, LILACS, and GOOGLE ACADEMIC. The following descriptors (DeCS) were used: "Autistic Spectrum Disorder"; "Gastrointestinal microbiota"; "Dysbiosis", associated with the Boolean operator "AND". We included literature review articles, complete, original, limited to English and Brazilian Portuguese languages, published in the last five years, and which, after reading the abstract, were within the scope of the review. Results: 52 manuscripts were identified, and after applying the inclusion and exclusion criteria, 11 articles were considered that show the worsening of ASD due to factors intrinsic to the intestinal microbiota. Conclusion: there is an important causal influence of the bidirectional brain-gut-microbiota axis in the etiology and exacerbation of clinical manifestations of Autism Spectrum Disorder due to intestinal dysbiosis and gastrointestinal factors of idiopathic origin.

Microbiota intestinal en la salud humana / Gut microbiota in human health

Introducción: La microbiota describe a un grupo de microorganismos en una región o período de tiempo que incluye: bacterias, arqueas, protistas, hongos y virus. Objetivos: Explicar la función de la microbiota intestinal en la salud humana. Métodos: Se realizó una búsqueda en diferentes de bases de datos como NHI, Ebsco y PubMed en idioma español e inglés, se revisó un total de 17 artículos de los cuales el mayor por ciento es de menos de 5 años. Resultados: Las microbiota intestinal en su mayoría se compone de Gram negativa, con una pared celular rica en lipopolisacáridos (LPS) que potencia a la inmunidad innata por interacción de receptor Toll-like (TLR) ligando, desencadena la producción de citoquinas proinflamatorias, entre otros. Conclusiones: La microbiota intestinal funciona como un señalizador antiinflamatorio y regulador de la permeabilidad epitelial intestinal(AU)

Introduction: Microbiota describes a group of microorganisms in a region or period of time that includes bacteria, archaea, protists, fungi, and viruses. Objectives: To explain the role of the intestinal microbiota in human health. Methods: A search was carried out in different databases such as NHI, Ebsco and PubMed in Spanish and English, a total of 17 articles were reviewed, most of them are less than 5 years. Results: Intestinal microbiota is mostly composed of Gram negative, with a cell wall rich in lipopolysaccharides (LPS) that enhances innate immunity by Toll-like receptor (TLR) ligand interaction, triggers the production of proinflammatory cytokines, among others. Conclusions: Intestinal microbiota functions as an anti-inflammatory signaling agent and regulator of intestinal epithelial permeability(AU)

Disbiosis bacteriana y su efecto en enfermedades bucales: una revisión bibliográfica / Bacterial dysbiosis and its effect on oral diseases: a review bibliographic

Objetivo: actualizar la información sobre la disbiosis bacteriana oral y su efecto en enfermedades bucales. Material y métodos: se realizó una revisión bibliográfica detallada, donde la búsqueda de artículos comenzó desde el 2014 con trabajos de investigación relacionados con el tema. Se aplicaron palabras clave para facilitar y delimitar el tema. En los resultados obtenidos se observa información específica de disbiosis bacteriana y los problemas y enfermedades que causan en la cavidad bucal. Conclusión: la cavidad oral es un ecosistema muy complejo e interactivo donde se desarrollan variedades de hábitats que establecen relaciones entre los microorganismos en los distintos medios bucales. Por lo general, el cuerpo humano vive en simbiosis con dichas bacterias, esta relación hospedador-huésped es producto de años de evolución y convivencia para poder tolerar a dichas especies y por medio de años de investigación, determinar a los agentes patógenos y a los simbióticos, lo que permitirá en un futuro tener enfoques terapéuticos y científicos, para así solucionar, mejorar y evitar problemas relacionados con la salud (AU)

Objective: this review aimed to update the information on oral bacterial dysbiosis and its effect on oral diseases. Material and methods: a detailed literature review was performed, where the search for articles began in 2014 with research papers related to the topic. Keywords were applied to facilitate and delimit the topic. The results obtained show specific information on bacterial dysbiosis and the problems and diseases they cause in the oral cavity. Conclusion: the oral cavity is a very complex and interactive ecosystem where a variety of habitats develop and establish relationships between microorganisms in different oral environments. Generally, the human body lives in symbiosis with these bacteria, this host-guest relationship is the product of years of evolution and coexistence to be able to tolerate these species and through years of research to determine the pathogens and symbiotics, which will allow in the future to have therapeutic and scientific approaches, to solve, improve and avoid health-related problems (AU)

Microbiota intestinal y modulación del tejido adiposo en la patogénesis de la obesidad / Gut microbiota and modulation of adipose tissue in the pathogenesis of obesity

Las investigaciones realizadas durante el último siglo relacionadas con la descripción de la Microbiota Intestinal (MI) sugieren una relación concreta entre su composición y la salud del huésped. Su desregulación denominada disbiosis intestinal ha sido asociada a distintos tipos de enfermedades gastrointestinales, metabólicas, oncológicas e incluso psiquiátricas. Destacan numerosos reportes que han informado la condición de disbiosis en la obesidad, tanto en modelos animales como humanos de distintos grupos etarios y regiones del mundo. A su vez, la composición del microbioma también ha logrado asociarse a las diferentes comorbilidades de la obesidad, postulando que la MI posee influencia en la disfunción del tejido adiposo (TA), entendiendo que corresponde al principal modulador de la patogénesis de la obesidad. Sin embargo, aún no es posible establecer una explicación mecanicista plausible. Actualmente, la utilización de tecnologías multiómicas, junto con la evaluación de variables fisiológicas, nos podrían proporcionar una mejor comprensión a la incógnita planteada. Frente a esto, el presente trabajo tiene como objetivo revisar los últimos avances en la comprensión de la influencia de la microbiota intestinal en el TA y su contribución a los mecanismos relacionados con la patogénesis de la obesidad. Entre los principales mecanismos identificados, la evidencia reporta nexos fisiológicos entre la composición de la MI y la modulación de inflamación, permeabilidad intestinal y adipogénesis. Las vías implicadas derivan de la influencia de la disbiosis intestinal en el accionar de ácidos grasos de cadena corta, claudinas, macrófagos, oligosacáridos, entre otros. Los mecanismos implicados, principalmente estudiados en modelos animales, deberían ser considerados para su evaluación en próximos estudios longitudinales y experimentales en humanos con el fin de obtener una mayor comprensión sobre la implicancia de cada mecanismo en la patogenia global de la obesidad(AU)

The investigations carried out during the last century related to the description of the Gut Microbiota (GM) suggest a concrete relationship between its composition and the health of the host. Its deregulation called intestinal dysbiosis has been associated with different types of gastrointestinal, metabolic, oncological and even psychiatric diseases. Numerous reports that have described the condition of dysbiosis in obesity stand out, both in animal and human models of different age groups and regions of the world. In turn, the composition of the microbiome has also been associated with the different comorbidities of obesity, postulating that MI has an influence on adipose tissue (AT) dysfunction, understanding that it corresponds to the main modulator of the pathogenesis of obesity. However, it is not yet possible to establish a plausible mechanistic explanation. Currently, the use of multi-omics technologies, together with the evaluation of physiological variables, could provide us with a better understanding of the question raised. In view of this, this review aims to review the latest advances in understanding the influence of the intestinal microbiota on AT and its contribution to the mechanisms related to the pathogenesis of obesity. Among the main mechanisms identified, the evidence reports physiological links between the composition of GM and the modulation of inflammation, intestinal permeability and adipogenesis. The pathways involved derive from the influence of intestinal dysbiosis on the action of short-chain fatty acids, claudins, macrophages, oligosaccharides, among others. The mechanisms involved, mainly studied in animal models, should be considered for evaluation in future longitudinal and experimental studies in humans in order to obtain a better understanding of the implication of each mechanism in the global pathogenesis of obesity(AU)

Metabolitos bioactivos generados por la disbiosis intestinal y sus implicaciones fisiopatológicas en la enfermedad cardiovascular / Bioactive metabolites generated by intestinal dysbiosis and their pathophysiological implications in cardiovascular disease

Introducción: La disbiosis conocida como la alteración de la relación simbiótica entre la microbiota intestinal y el huésped están implicados en la patogenia de la enfermedad cardiovascular aterosclerótica. Objetivo: Realizar una revisión documental sobre los mecanismos fisiopatológicos que relacionan los metabolitos bioactivos generados por la disbiosis intestinal con el desarrollo y progresión de la enfermedad cardiovascular aterosclerótica. Métodos: Se utilizó el motor de búsqueda Google Académico y se consultaron artículos de libre acceso en las bases de datos Pubmed, SciELO, Lilacs, Cumed y Hinari desde septiembre 2020 hasta el mes de marzo 2021. Las palabras clave utilizadas para esta revisión fueron:microbioma, microbiota intestinal, disbiosis, aterosclerosis, enfermedad cardiovascular y sus equivalentes en inglés, según el descriptor de Ciencias de la Salud (DeCS). Se consideraron artículos originales, de revisión, revisiones sistemáticas y metaanálisis posteriores al año 2015. Se revisaron un total de 73 artículos. Desarrollo: Las relaciones fisiopatológicas entre la disbiosis intestinal y las enfermedades cardiovasculares son complejas, ya que se influyen mutuamente a través de los sus toxinas endógenas (metabolitos bioactivos), el sistema circulatorio, las respuestas inmunitarias y los cambios metabólicos. Las investigaciones futuras deberían centrarse en dilucidar los actores moleculares subyacentes e identificar si las vías que interconectan la disbiosis intestinal con la ECA son causales, correlacionales o consecuentes. Conclusiones: La evidencia acumulada sostiene que la disbiosis de la microbiota intestinal está involucrada en la síntesis de metabolitos proaterogénicos los cuales modulan los mecanismos implicados en la fisiopatología de la ECA(AU)

Introduction: Dysbiosis is known as the alteration of the symbiotic relationship between the intestinal microbiota and the host is involved in the pathogenesis of atherosclerotic cardiovascular disease. Objective: To carry out a documentary review on the pathophysiological mechanisms that relate the bioactive metabolites generated by intestinal dysbiosis with the development and progression of atherosclerotic cardiovascular disease. Methods: The Google Scholar search engine was used and free access articles were consulted in Pubmed, SciELO, Lilacs, Cumed and Hinari databases from September 2020 to March 2021. The keywords used for this review were microbiome, gut microbiota, dysbiosis, atherosclerosis, cardiovascular disease and their English equivalents, according to the Health Sciences (DeCS) descriptor. Original articles, review articles, systematic reviews and meta-analyses after 2015 were considered. A total of 73 articles were reviewed. Findings: The pathophysiological relationships between intestinal dysbiosis and cardiovascular diseases are complex, since they influence each other through their endogenous toxins (bioactive metabolites), the circulatory system, immune responses and metabolic changes. Future research should focus on elucidating the underlying molecular players and on identifying whether the pathways that interconnect gut dysbiosis with ACE are causal, correlational, or consequential. Conclusions: The accumulated evidence supports that the dysbiosis of the intestinal microbiota is involved in the synthesis of proatherogenic metabolites which modulate the mechanisms involved in the pathophysiology of ACE(AU)

Modulación inmune en enfermedades alérgicas asociada al uso de Bifidobacterium en menores de cinco años / Immune modulation in allergic diseases associated with the use of Bifidobacterium in children under five years of age

La incidencia de enfermedades alérgicas en la infancia va en aumento, y se ha convertido en una de las principales consultas. Una posible causa es la disbiosis del microbioma intestinal, relacionada con estados inflamatorios aumentados. Debido a la necesidad de mejorar la calidad de vida, y el impacto en lo económico y en lo educativo, surgen los probióticos como tratamiento adyuvante, por lo que se pretende determinar la asociación del uso de Bifidobacterium en menores de 5 años con la modulación de la respuesta inmune en enfermedades alérgicas. El microbioma intestinal inicia su desarrollo y maduración desde la gestación, continúa en el nacimiento y termina hasta los 3 años, influenciado por factores maternos, neonatales y ambientales. La disbiosis intestinal generada por estos factores reduce la proporción de bifidobacterias, lo cual se relaciona con estados proinflamatorios. En consecuencia, estudios del uso de Bifidobacterium en niños con enfermedades alérgicas ha evidenciado mejora de síntomas y calidad de vida. Los probióticos favorecen un microbioma intestinal saludable, asociado a un estado antiinflamatorio, debido a la regulación en el balance celular Th1/Th2/T reguladoras y células asesinas naturales. Esta modulación en la respuesta inmune permite mejor control de síntomas, calidad de vida y menor incidencia de enfermedades alérgicas en la infancia

The incidence of allergic diseases in childhood is increasing, and has become one of the main queries. One possible cause is dysbiosis of the gut microbiome, related to increased inflammatory states. Due to the need to improve the quality of life, and the economic and educational impact, probiotics emerge as adjuvant treatment, so it is intended to determine the association of the use of Bifidobacterium in children under 5 years with the modulation of the immune response in allergic diseases. The intestinal microbiome begins its development and maturation from gestation, continues at birth and ends up to 3 years, influenced by maternal, neonatal and environmental factors. The intestinal dysbiosis generated by these factors reduces the proportion of bifidobacteria, which is related to proinflammatory states. Consequently, studies of the use of Bifidobacterium in children with allergic diseases have shown improvement in symptoms and quality of life. Probiotics favor a healthy intestinal microbiome, associated with an anti-inflammatory state, due to the regulation of the regulatory Th1/Th2/T cell balance and natural killer cells. This modulation in the immune response allows better control of symptoms, quality of life and lower incidence of allergic diseases in childhood

Can periodontitis affect colorectal cancer by altering microbiota balance? / 中华口腔医学杂志

Emerging evidence suggests that, along with dietary, genetic and environmental factors, gut microbiota plays a role in the progress of colorectal cancer. Dysbiosis of oral flora in patients with periodontitis affects the composition of microbial community in the gut, impairs gut barrier function, and induces a proinflammatory microenvironment, all of which contribute to the progression of colorectal cancer. In view of the influences by microbiota dysbiosis, this article reviews the role of periodontitis in affecting the occurrence and development of colorectal cancer.

Dendrobium nobile protects against ovalbumin-induced allergic rhinitis by regulating intestinal flora and suppressing lung inflammation / 中国天然药物

Antibiotic exposure-induced dysbiosis of the intestinal flora increases the risk of developing allergic rhinitis. Hence, regulating the balance of intestinal flora may be useful for preventing and treating allergic rhinitis. However, the underlying mechanism is unclear. Dendrobium nobile (Shihu) exhibits anti-inflammatory and immune activities. Hence, in this study, we investigated the mechanism via which Shihu may improve allergic rhinitis. Mouse models of allergic rhinitis with intestinal flora dysbiosis (Model-D, antibiotics induce intestinal flora dysbiosis with ovalbumin-induced allergy) and normal intestinal flora with allergic rhinitis (Model-N, ovalbumin-induced allergy) were established. The effect of Shihu on intestinal flora and inflammation caused during allergic rhinitis were analyzed. Allergic symptoms, infiltration of hematoxylin and eosin in the lungs and nose, and the release of various factors [interleukin (IL)-2, IL-4, IFN-γ, IL-6, IL-10, and IL-17] in the lungs were evaluated. The results indicate that intestinal flora dysbiosis exacerbated lung and nose inflammation in allergic rhinitis. However, treatment with the Shihu extract effectively reversed these symptoms. Besides, the Shihu extract inhibited the PI3K/AKT/mTOR pathway and increased the level of Forkhead box protein in the lungs. Additionally, the Shihu extract reversed intestinal flora dysbiosis at the phylum and genus levels and improved regulator T cell differentiation. Furthermore, in the Model-D group, the Shihu extract inhibited the decrease in the diversity and abundance of the intestinal flora. Screening was performed to determine which intestinal flora was positively correlated with Treg differentiation using Spearman's correlation analysis. In conclusion, we showed that Shihu extract restored the balance in intestinal flora and ameliorated inflammation in the lungs of allergic rhinitis mice and predicted a therapeutic new approach using Traditional Chinese Medicine to improve allergic rhinitis.