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1.
J Hazard Mater ; 441: 129903, 2023 01 05.
Artigo em Inglês | MEDLINE | ID: mdl-36087528

RESUMO

Microplastics (MP) and nanoplastics (NP) exist in the disposable plastic take-away containers. This study aims to determine the gut and oral microbiota alterations in the individuals frequently and occasionally consuming take-away food in disposable plastic containers (TFDPC), and explore the effect of micro/nanoplastics (MNP) reduction on gut microbiota in mice. TFDPC consumption are associated with greater presences of gastrointestinal dysfunction and cough. Both occasional and frequent consumers have altered gut and oral microbiota, and their gut diversity and evenness are greater than those of non-TFDPC consuming cohort. Multiple gut and oral bacteria are associated with TFDPC consumers, among which intestinal Collinsella and oral Thiobacillus are most associated with the frequent consumers, while intestinal Faecalibacterium is most associated with the occasional consumers. Although some gut bacteria associated with the mice treated with 500 µg NP and 500 µg MP are decreased in the mice treated with 200 µg NP, the gut microbiota of the three MNP groups are all different from the control group. This study demonstrates that TFDPC induces gut and oral microbiota alterations in the consumers, and partial reduction of the size and amount of MNP cannot rectify the MNP-induced gut microbial dysbiosis.


Assuntos
Microbioma Gastrointestinal , Microbiota , Animais , Disbiose/induzido quimicamente , Camundongos , Microplásticos , Plásticos/toxicidade
2.
Braz. j. biol ; 83: e242818, 2023. tab, graf
Artigo em Inglês | LILACS, VETINDEX | ID: biblio-1285628

RESUMO

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.


Assuntos
Humanos , Animais , Coelhos , Diabetes Mellitus Tipo 2 , Microbioma Gastrointestinal , Bacteroides , RNA Ribossômico 16S/genética , Prevotella , Bacteroidetes , Ruminococcus , Dieta Hiperlipídica/efeitos adversos , Disbiose , Inflamação , Camundongos Endogâmicos C57BL
3.
Chemosphere ; 310: 136764, 2023 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-36216111

RESUMO

Microplastics (MP) and nanoplastics (NP) have been found in multiple environments and creatures. However, their effects on the airway microbiota still remain poorly understood. In this study, a series of bioinformatic and statistical analyses were carried out to explore the influence of airborne MP and NP on the nasal and lung microbiota in mice. Both MP and NP were capable of inducing nasal microbial dysbiosis, and MP had a stronger influence on the lung microbiota than NP. Multiple nasal and lung bacteria were associated with MP and NP groups, among which nasal Staphylococcus and lung Roseburia were most associated with MP group, while nasal Prevotella and lung unclassified_Muribaculaceae were most associated with NP group. The nasal Staphylococcus, lung Roseburia, lung Eggerthella and lung Corynebacterium were associated with both MP and NP groups, which were potential biomarkers of micro/nanoplastics-induced airway dysbiosis. SAR11_Clade_Ia and SAR11_Clade_II were associated with both nasal and lung microbiota in MP group, while no such bacterium was determined in NP group. The relevant results suggest that both airborne MP and NP could induce nasal and lung microbial dysbiosis, and the relevant preventative and curable strategies deserve further investigations.


Assuntos
Disbiose , Microplásticos , Camundongos , Animais , Disbiose/induzido quimicamente , Microplásticos/toxicidade , Poliestirenos , Plásticos/toxicidade , Pulmão
4.
Artigo em Inglês | MEDLINE | ID: mdl-36174907

RESUMO

Nanotechnology has revealed profound possibilities for the applications in applied sciences. The nanotechnology works based on nanoparticles. Among nanoparticles, silver nanoparticles largely introduced into aquatic environments during fabrication. Which cause severe contamination in the environment specially in freshwater fish. Therefore, the current study was a pioneer attempt to use the animal blood to fabricate AgNPs and investigate their toxicity in Cyprinus carpio (C. carpio) by recording mortality, tissue bioaccumulation, and influence on intestinal bacterial diversity. For this purpose, fish groups were exposed to different concentrations of B-AgNPs including 0.03, 0.06, and 0.09 mg/L beside the control group for 1, 10, and 20 days. Initially, the highest concentration caused mortality. The results revealed that B-AgNPs were significantly (p < 0.005) accumulated in the liver followed by intestines, gills, and muscles. In addition, the accumulation of B-AgNPs in the intestine led to bacterial dysbiosis in Cyprinus carpio. At the phylum level, Tenericutes, Bacteroidetes, and Planctomycetes were gradually decreased at the highest concentration of B-AgNPs (0.09 mg/L) on days 1, 10, and 20 days. The genera Cetobacterium and Luteolibactor were increased at the highest concentration on day 20. Moreover, the principal coordinate analysis (PCoA) based on Bray-Curtis showed that the B-AgNPs had led to a variation in the intestinal bacterial community. Based on findings, the B-AgNPs induced mortality, and residual deposition in different tissues, and had a stress influence on intestinal homeostasis by affecting the intestinal bacterial community in C. carpio which could have a significant effect on fish growth.


Assuntos
Carpas , Nanopartículas Metálicas , Poluentes Químicos da Água , Animais , Prata/toxicidade , Nanopartículas Metálicas/toxicidade , Disbiose/induzido quimicamente , Brânquias , Bactérias , Poluentes Químicos da Água/toxicidade
5.
Microbiol Res ; 266: 127244, 2023 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-36335803

RESUMO

Though it has been widely accepted that infections of the respiratory tract is associated with aetiology of acute exacerbation of chronic obstructive pulmonary disease (AECOPD), more recent techniques have shown emerging evidence on the importance of alterations of diversity and composition of microbiota itself in the disease process. Specifically, these alterations is widely present in COPD patients from a variety of populations, and is associated with severity of disease, frequency of acute exacerbation, as well as prediction of exacerbation. In addition, the microbiota from respiratory tract contributes to disease mechanisms, and more recently have been shown to interact with gut microbiota in a bidirectional way. Therefore, updating progress in the field is crucial as it not only reveals potential underlying mechanisms of the disease, but also highlights the potential utilisation of microbiota as a biomarker for disease prediction and as a target for treatment. In this narrative review, we summarize current updates on microbiota dysbiosis in COPD, including techniques for sampling and analysis of microbiota, recent findings on the presence of microbiota dysbiosis and its correlation with clinical prediction and prognosis of the disease, as well as its potential roles in disease mechanisms. In addition, how gut-lung axis contributes to COPD progression is also discussed. Finally, we addressed the utilisation of prebiotic and probiotic treatment for COPD. Together, we hope to provide useful information to advocate the use of microbial parameters as important tools for diagnosis, treatment and long-term follow-up for COPD patients.


Assuntos
Microbiota , Doença Pulmonar Obstrutiva Crônica , Humanos , Disbiose , Progressão da Doença , Doença Pulmonar Obstrutiva Crônica/tratamento farmacológico , Pulmão
6.
J Intensive Care Med ; 38(1): 121-131, 2023 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-35603752

RESUMO

Sepsis, as an important public health concern, is one of the leading causes of death in hospitals around the world, accounting for 25% of all deaths. Nowadays, several factors contribute to the development of sepsis. The role of the gut microbiota and the response state of the aberrant immune system is dominant. The effect of the human microbiome on health is undeniable, and gut microbiota is even considered a body organ. It is now clear that the alteration in the normal balance of the microbiota (dysbiosis) is associated with a change in the status of immune system responses. Owing to the strong association between the gut microbiota and its metabolites particularly short-chain fatty acids with many illnesses, the gut microbiota has a unique position in the research of microbiologists and even clinicians. This review aimed to analyze studies' results on the association between microbiota and sepsis, with a substantial understanding of their relationship. As a result, an extensive and comprehensive search was conducted on this issue in existing databases.


Assuntos
Microbioma Gastrointestinal , Microbiota , Sepse , Humanos , Microbioma Gastrointestinal/fisiologia , Disbiose , Sistema Imunitário
7.
J Nutr Biochem ; 111: 109188, 2023 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-36272693

RESUMO

Adoption of an obesogenic diet such as a high-fat diet (HFD) results in obesity, bacterial dysbiosis, chronic inflammation, and cancer. Gut bacteria and their metabolites are recognized by interleukin-1 (IL-1R)/toll-like receptors (TLRs) which are essential to maintain intestinal homeostasis. Moreover, host extracellular microRNAs (miRNAs) can alter bacterial growth in the colon. Characterization of the underlying mechanisms may lead to identifying fecal oncogenic signatures reflecting colonic health. We hypothesize that an HFD accelerates the inflammatory process and modulates IL-1R/TLR pathways, gut microbiome, and disease-related miRNA in the colon. In this study, 4-week-old C57BL/6 mice were fed a modified AIN93G diet (AIN, 16% energy fat) or an HFD (45% energy fat) for 15 weeks. In addition to increased body weight and body fat composition, the concentrations of plasma interleukin 6 (IL-6), inflammatory cell infiltration, ß-catenin, and cell proliferation marker (Ki67) in the colon were elevated > 68% in the HFD group compared to the AIN group. Using a PCR array analysis, we identified 14 out of 84 genes with a ≥ 24% decrease in mRNA content related to IL-1R and TLR pathways in colonic epithelial cells in mice fed an HFD compared to the AIN. Furthermore, the content of Alistipes bacteria, the Firmicutes/Bacteroidetes ratio, microRNA-29a, and deoxycholic and lithocholic acids (secondary bile acids with oncogenic potential) were 55% greater in the feces of the HFD group compared to the AIN group. Collectively, this composite, a multimodal profile may represent a unique HFD-induced fecal signature for colonic inflammation and cancer in C57BL/6 mice.


Assuntos
Dieta Hiperlipídica , Disbiose , Camundongos , Animais , Dieta Hiperlipídica/efeitos adversos , Camundongos Endogâmicos C57BL , Disbiose/microbiologia , Colo/metabolismo , Inflamação/metabolismo , Bactérias
8.
Ann Clin Microbiol Antimicrob ; 21(1): 46, 2022 Nov 03.
Artigo em Inglês | MEDLINE | ID: mdl-36329476

RESUMO

BACKGROUND: Early-life antibiotic exposure is associated with the development of later obesity through the disruption of gut microbiota in the animal models. However, the related epidemiological evidence is still conflicting. METHODS: A birth cohort was consisted of 2140 mother-infant pairs in Chaoyang District Maternal and Child Health Care Hospital in this study. Here, their available antibiotic exposure during the first one year of life was ascertained using a open-ended questionnaire and related anthropometric parameters from the health screening program. The compositions of gut microbiota were comprehensively analyzed by16S rRNA high throughput sequencing. Then the spearman correlations were performed by the multiple covariance-adjusted regressions between the antibiotic exposure with anthropometric parameters and compositions of gut microbiota. RESULTS: Among the 2140 subjects, the antibiotic exposure during the first one year of life was 53.04%, mainly by Cephalosporins (53.39%) and Erythromycins(27.67%) for the treatment of respiratory tract infection (79.56%), which were not significantly different among the subgroups. Compared to the control group, both childhood overweight and obesity at two and a half years were higher in the antibiotic exposed group, with higher percents of Faecalibacterium, Agathobacter and Klebsiella, and lower percentage of Bifidobacterium. Moreover, there were positively potential associations between early-life antibiotic exposure with the accelerated anthropometric parameters and disruption of Faecalibacterium, Agathobacter, Klebsiella and Bifidobacterium at two and a half years. CONCLUSION: These above results proved that early-life antibiotic exposure was positively associated with the accelerated childhood overweight and obesity from one year to two and a half years by impacting the disorders of Faecalibacterium, Agathobacter, Klebsiella and Bifidobacterium, which would propose the theoretical basis for rationalizing the personalized antibiotic exposure among the infants to truly reflect the fairness of public health.


Assuntos
Microbioma Gastrointestinal , Obesidade Pediátrica , Humanos , Animais , Disbiose , Obesidade Pediátrica/epidemiologia , Estudos de Coortes , Antibacterianos/efeitos adversos , Coorte de Nascimento , Klebsiella/genética
9.
Microbiome ; 10(1): 187, 2022 Nov 04.
Artigo em Inglês | MEDLINE | ID: mdl-36329549

RESUMO

BACKGROUND: Gut microbiota (GM) dysregulation, known as dysbiosis, has been proposed as a crucial driver of obesity associated with "Western" diet (WD) consumption. Gut dysbiosis is associated with increased gut permeability, inflammation, and insulin resistance. However, host metabolic pathways implicated in the pathophysiology of gut dysbiosis are still elusive. Exchange protein directly activated by cAMP (Epac) plays a critical role in cell-cell junction formation and insulin secretion. Here, we used homozygous Epac1-knockout (Epac1-/-), Epac2-knockout (Epac2-/-), and wild-type (WT) mice to investigate the role of Epac proteins in mediating gut dysbiosis, gut permeability, and inflammation after WD feeding. RESULTS: The 16S rRNA gene sequencing of fecal DNA showed that the baseline GM of Epac2-/-, but not Epac1-/-, mice was represented by a significantly higher Firmicutes to Bacteroidetes ratio and significant alterations in several taxa compared to WT mice, suggesting that Epac2-/- mice had gut dysbiosis under physiological conditions. However, an 8-week WD led to a similar gut microbiome imbalance in mice regardless of genotype. While Epac1 deficiency modestly exacerbated the WD-induced GM dysbiosis, the WD-fed Epac2-/- mice had a more significant increase in gut permeability than corresponding WT mice. After WD feeding, Epac1-/-, but not Epac2-/-, mice had significantly higher mRNA levels of tumor necrosis factor-alpha (TNF-α) and F4/80 in the epididymal white adipose tissue (EWAT), increased circulating lipocalin-2 protein and more severe glucose intolerance, suggesting greater inflammation and insulin resistance in WD-fed Epac1-/- mice than corresponding WT mice. Consistently, Epac1 protein expression was significantly reduced in the EWAT of WD-fed WT and Epac2-/- mice. CONCLUSION: Despite significantly dysregulated baseline GM and a more pronounced increase in gut permeability upon WD feeding, WD-fed Epac2-/- mice did not exhibit more severe inflammation and glucose intolerance than corresponding WT mice. These findings suggest that the role of gut dysbiosis in mediating WD-associated obesity may be context-dependent. On the contrary, we demonstrate that deficiency of host signaling protein, Epac1, drives inflammation and glucose intolerance which are the hallmarks of WD-induced obesity. Video abstract.


Assuntos
Intolerância à Glucose , Resistência à Insulina , Animais , Camundongos , Dieta Ocidental , Disbiose , Fatores de Troca do Nucleotídeo Guanina/genética , Fatores de Troca do Nucleotídeo Guanina/metabolismo , Inflamação , Camundongos Endogâmicos C57BL , Obesidade/etiologia , RNA Ribossômico 16S/genética
10.
Microb Cell Fact ; 21(1): 241, 2022 Nov 23.
Artigo em Inglês | MEDLINE | ID: mdl-36419034

RESUMO

Recent studies have demonstrated that gut microbiota plays critical roles in various human diseases. High-throughput technology has been widely applied to characterize the microbial ecosystems, which led to an explosion of different types of molecular profiling data, such as metagenomics, metatranscriptomics and metabolomics. For analysis of such data, machine learning algorithms have shown to be useful for identifying key molecular signatures, discovering potential patient stratifications, and particularly for generating models that can accurately predict phenotypes. In this review, we first discuss how dysbiosis of the intestinal microbiota is linked to human disease development and how potential modulation strategies of the gut microbial ecosystem can be used for disease treatment. In addition, we introduce categories and workflows of different machine learning approaches, and how they can be used to perform integrative analysis of multi-omics data. Finally, we review advances of machine learning in gut microbiome applications and discuss related challenges. Based on this we conclude that machine learning is very well suited for analysis of gut microbiome and that these approaches can be useful for development of gut microbe-targeted therapies, which ultimately can help in achieving personalized and precision medicine.


Assuntos
Microbioma Gastrointestinal , Microbiota , Humanos , Metagenômica , Disbiose , Aprendizado de Máquina
11.
Gut Microbes ; 14(1): 2143225, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-36409161

RESUMO

The gut microbial ecosystem exhibits a complex bidirectional communication with the host and is one of the key contributing factors in determining mucosal immune homeostasis or an inflammatory state. Opioid use has been established to induce gut microbial dysbiosis consistent with increased intestinal tissue inflammation. In this study, we investigated the role of infiltrated immune cells in morphine-induced intestinal tissue damage and gut microbial dysbiosis in mice. Results reveal a significant increase in chemokine expression in intestinal tissues followed by increased neutrophil infiltration post morphine treatment which is direct consequence of a dysbiotic microbiome since the effect is attenuated in antibiotics treated animals and in germ-free mice. Neutrophil neutralization using anti-Ly6G monoclonal antibody showed a significant decrease in tissue damage and an increase in tight junction protein organization. 16S rRNA sequencing on intestinal samples highlighted the role of infiltrated neutrophils in modulating microbial community structure by providing a growth benefit for pathogenic bacteria, such as Enterococcus, and simultaneously causing a significant depletion of commensal bacteria, such as Lactobacillus. Taken together, we provide the first direct evidence that neutrophil infiltration contributes to morphine-induced intestinal tissue damage and gut microbial dysbiosis. Our findings implicate that inhibition of neutrophil infiltration may provide therapeutic benefits against gastrointestinal dysfunctions associated with opioid use.


Assuntos
Microbioma Gastrointestinal , Microbiota , Transtornos Relacionados ao Uso de Opioides , Animais , Camundongos , Infiltração de Neutrófilos , Disbiose/induzido quimicamente , Morfina , Analgésicos Opioides , RNA Ribossômico 16S/genética
12.
Cell Rep ; 41(8): 111681, 2022 Nov 22.
Artigo em Inglês | MEDLINE | ID: mdl-36417859

RESUMO

The precise mechanism by which gut dysbiosis contributes to the pathogenesis of extraintestinal diseases and how commensal microbes mediate these processes remain unclear. Here, we show that cows with mastitis had marked gut dysbiosis, characterized by the enrichment of opportunistic pathogenic Escherichia_Shigella and the depletion of commensal Roseburia. Fecal microbiota transplantation from donor cows with mastitis (M-FMT) to recipient mice significantly caused mastitis and changed the gut and mammary microbiota in mice. Notably, M-FMT facilitated the translocation of pathobiont from the gut into the mammary gland, and the depletion of Enterobacteriaceae alleviated M-FMT-induced mastitis in mice. In contrast, commensal Roseburia intestinalis improved M-FMT-induced mastitis and microbial dysbiosis in the gut and mammary gland and limited bacterial translocation by producing butyrate, which was associated with inflammatory signaling inhibition and barrier repair. Our research suggests that commensal Roseburia alleviates gut-dysbiosis-induced mastitis, although further studies in dairy cows and humans are needed.


Assuntos
Microbioma Gastrointestinal , Mastite , Feminino , Bovinos , Camundongos , Animais , Humanos , Disbiose/complicações , Translocação Bacteriana , Butiratos/farmacologia , Microbioma Gastrointestinal/fisiologia , Mastite/complicações
13.
Biomed Pharmacother ; 156: 113949, 2022 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-36411634

RESUMO

Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder with a rapidly increasing global prevalence. Early unstable and immature microbiota are often observed in ASD patients, resulting in neurobehavioral dysfunction. Since the establishment of stable gut microbiota in early life falls into the same critical time window as neurodevelopment, manipulations of the gut microbiota during early life could become a promising strategy for ASD. Melatonin is an endogenous hormone and can restore gut microbial dysbiosis under various disease conditions. Here, we explored the effects of melatonin supplementation during early life on the gut microbiota of the offspring and the subsequent impact on ASD-associated behaviors. Using the valproic acid (VPA) - induced mouse model of autism, we found that melatonin supplementation during late gestation and early postnatal development rescued the social deficits of the offspring. In addition, melatonin restored gut microbial dysbiosis in the VPA-exposed offspring, which was characterized by the significant upregulation of Akkermansia spp. Furthermore, supplementation of Akkermansia spp. alleviated the social deficits induced by VPA exposure via activating the dopaminergic neurons in the ventral tegmental area. These findings discover a novel mechanism underlying the gut microbiota regulation of social behaviors and provide the biological basis for developing gut microbiota-based therapeutics for ASD.


Assuntos
Transtorno do Espectro Autista , Transtorno Autístico , Microbioma Gastrointestinal , Melatonina , Camundongos , Gravidez , Animais , Feminino , Transtorno Autístico/tratamento farmacológico , Melatonina/farmacologia , Melatonina/uso terapêutico , Disbiose/tratamento farmacológico , Transtorno do Espectro Autista/tratamento farmacológico , Modelos Animais de Doenças , Akkermansia , Ácido Valproico/farmacologia , Suplementos Nutricionais
14.
Cell Rep ; 41(7): 111637, 2022 Nov 15.
Artigo em Inglês | MEDLINE | ID: mdl-36384110

RESUMO

Endoplasmic reticulum (ER) stress is associated with Crohn's disease (CD), but its impact on host-microbe interaction in disease pathogenesis is not well defined. Functional deficiency in the protein disulfide isomerase anterior gradient 2 (AGR2) has been linked with CD and leads to epithelial cell ER stress and ileocolitis in mice and humans. Here, we show that ileal expression of AGR2 correlates with mucosal Enterobactericeae abundance in human inflammatory bowel disease (IBD) and that Agr2 deletion leads to ER-stress-dependent expansion of mucosal-associated adherent-invasive Escherichia coli (AIEC), which drives Th17 cell ileocolitis in mice. Mechanistically, our data reveal that AIEC-induced epithelial cell ER stress triggers CD103+ dendritic cell production of interleukin-23 (IL-23) and that IL-23R is required for ileocolitis in Agr2-/- mice. Overall, these data reveal a specific and reciprocal interaction of the expansion of the CD pathobiont AIEC with ER-stress-associated ileocolitis and highlight a distinct cellular mechanism for IL-23-dependent ileocolitis.


Assuntos
Doença de Crohn , Disbiose , Infecções por Escherichia coli , Mucoproteínas , Animais , Humanos , Camundongos , Doença de Crohn/genética , Doença de Crohn/microbiologia , Células Dendríticas , Escherichia coli , Interleucina-23 , Mucoproteínas/genética , Proteínas Oncogênicas
15.
Front Endocrinol (Lausanne) ; 13: 1041647, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-36387894

RESUMO

The interaction between the gut microbiota and the host has been described experimentally by germ-free animals or by antibiotic-disturbed gut microbiota. Studies on germ-free mice have shown that gut microbiota is critical for bone growth and development in mice, emphasizing that microbiota dysbiosis may interfere with normal bone development processes. This study aimed to clarify the effect of antibiotic treatment on disturbed gut microbiota on bone development in mice and to investigate the effect of probiotic treatment on fracture healing in mice with dysbiosis. Our results showed that 4 weeks old female Kunming mice showed significantly lower abundance and diversity of the gut microbiota and significantly lower bone mineral density after 12 weeks of antibiotic treatment and significantly increased levels of RANKL and Ang II in serum (p<0.05). Mice with dysbiosis received 5 mL of Lactobacillus casei fermented milk by daily gavage after internal fixation of femoral fractures, and postoperative fracture healing was evaluated by X-ray, micro-CT scan, and HE staining, which showed faster growth of the broken ends of the femur and the presence of more callus. Serological tests showed decreased levels of RANKL and Ang II (p<0.05). Similarly, immunohistochemical results also showed increased expression of α smooth muscle actin in callus tissue. These results suggest that oral antibiotics can lead to dysbiosis of the gut microbiota in mice, which in turn leads to the development of osteoporosis. In contrast, probiotic treatment promoted fracture healing in osteoporotic mice after dysbiosis, and the probiotic effect on fracture healing may be produced by inhibiting the RAS/RANKL/RANK pathway.


Assuntos
Consolidação da Fratura , Lactobacillus casei , Camundongos , Feminino , Animais , Consolidação da Fratura/fisiologia , Leite , Disbiose , Camundongos Endogâmicos C57BL , Antibacterianos/farmacologia
16.
BMC Cancer ; 22(1): 1182, 2022 Nov 17.
Artigo em Inglês | MEDLINE | ID: mdl-36384523

RESUMO

BACKGROUND: Gut microbiome has been linked to a regulatory role in cancer progression. However, whether broad-spectrum antibiotics (ATB) associated gut microbiome dysbiosis contributes to an impaired T cell immune function, and ultimately promotes lung cancer metastasis is not well known. METHODS: In this study, a retrospective analysis was performed in a cohort of 263 patients initially diagnosed with non-small cell lung cancer (NSCLC) patients, including the ATB group (patients with broad-spectrum antibiotics treatment) (n = 124), and non-ATB group (n = 139) as control. ATB patients were prescribed ATB for over 5 days within 30 days prior to the collection of blood and fecal specimens and followed surgical treatment or first-line therapy. T cell immune function and metastasis-free survival (MFS) were evaluated between the two groups. Gut microbiota was evaluated by 16S rDNA sequencing. The predictive value of T cell immunity for MFS was evaluated by ROC analysis and Cox regression analysis. RESULTS: Our results suggest that broad-spectrum antibiotics (ATB) impair T cell immune function in patients with either early-stage or advanced NSCLC, which likely contribute to the promotion of lung cancer metastasis. Results of the survival analysis show that metastasis-free survival (MFS) is significantly shorter in the ATB patients than that in the non-ATB patients with stage III NSCLC. The 16S rDNA sequencing shows that ATB administration contributes to a significant dysbiosis of the composition and diversity of gut microbiota. Moreover, ROC analysis results of CD4 (AUC 0.642, p = 0.011), CD8 (AUC was 0.729, p < 0.001), CD16 + 56 + (AUC 0.643, p = 0.003), and the combination of CD4, CD8 and CD16 + 56+ (AUC 0.810, p < 0.001), or Cox regression analysis results of CD4 (HR 0.206, p < 0.001), CD8 (HR 0.555, p = 0.009), which is likely regulated by ATB administration, have significantly predictive values for MFS. CONCLUSION: These results provide evidence of gut microbiome disturbance due to ATB administration is involved in the regulation of T cell immunity, and their predictive value for the tumor metastasis in lung cancer patients. Thus, gut microbiota may serve as a therapeutic target for lung cancer. Consequently, caution should be exercised before the long-term administration of broad-spectrum antibiotics in cancer patients.


Assuntos
Carcinoma Pulmonar de Células não Pequenas , Microbioma Gastrointestinal , Neoplasias Pulmonares , Humanos , Neoplasias Pulmonares/patologia , Carcinoma Pulmonar de Células não Pequenas/patologia , Microbioma Gastrointestinal/fisiologia , Estudos Retrospectivos , Disbiose/induzido quimicamente , Antibacterianos/efeitos adversos , Processos Neoplásicos , Linfócitos T/patologia , DNA Ribossômico
17.
Front Cell Infect Microbiol ; 12: 1019789, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-36389146

RESUMO

Blastocystis is a genus of single-celled protist belonging to the stramenopile group. Prior studies have shown that isolates of Blastocystis subtype 7 (ST7) induced higher levels of intestinal epithelial cell damage and gut microbiota dysbiosis in comparison to other subtypes in in vivo and in vitro settings. Prior research has shown a link between gut dysbiosis and exposure to extracellular vesicles (EVs) produced by pathogenic microorganisms. This study demonstrates a protocol for the isolation of EVs from Blastocystis ST7 via ultracentrifugation. Nanoparticle tracking analysis and transmission electron microscopy were used to assess EV size and morphology. The protein content of isolated EVs was assessed by mass spectrophotometry and the presence of EV markers were evaluated by Western blotting. Finally, the EVs were cocultured with prominent human gut microbiome species to observe their effect on prokaryote growth. Our data shows that Blastocystis ST7 secretes EVs that are similar in morphology to previously characterized EVs from other organisms and that these EVs contain a limited yet unique protein cargo with functions in host-parasite intercellular communication and cell viability. This cargo may be involved in mediating the effects of Blastocystis on its surrounding environment.


Assuntos
Blastocystis , Vesículas Extracelulares , Parasitos , Animais , Humanos , Disbiose , Vesículas Extracelulares/metabolismo , Ultracentrifugação , Proteínas/metabolismo
18.
Front Cell Infect Microbiol ; 12: 1036946, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-36389150

RESUMO

Background: The incidence of early-onset colorectal cancer (EOCRC) is increasing worldwide. This study aimed to explore whether there is an alternative gut microbiota profile in patients with early-onset colorectal cancer. Methods: A total of 24 patients with EOCRC, 43 patients with late-onset colorectal cancer and 31 young volunteers were included in this study. The diversity of their fecal bacteria was explored using 16S ribosomal RNA gene sequencing. Cluster of ortholog genes (COG) functional annotation and Kyoto encyclopedia of genes and genomes (KEGG) were used to detect enrichment pathways among the three groups. Results: Community separations were observed among the three groups. The Shannon index of the EOCRC group was significantly lower than the LOCRC group (P=0.007) and the NC group (P=0.008). Both PCoA analysis (Principal co-ordinates analysis, P=0.001) and NMDS (non-metric multidimensional scaling, stress=0.167, P=0.001) analysis indicated significant difference in beta diversity among the three groups. Fusobacteria, Bacteroidetes, and Clostridia were the most abundant bacteria in the EOCRC group, LOCRC group, and NC group, respectively. The results of COG showed that transcription (P=0.01398), defense mechanisms (P=0.04304), inorganic ion transport and metabolism (P=0.00225) and cell wall/membrane/envelope biogenesis (P=0.02534) were differentially expressed among the three groups. The KEGG modules involved in membrane transport (P=0.00856) and porphyrin and chlorophyll metabolism (P=0.04909) were differentially expressed among the three groups. Conclusion: Early-onset colorectal cancer patients have a different gastrointestinal microbiota derangement compared to late-onset colorectal cancer patients. This dysbiosis can be reflected in the species diversity of the microbiota, the abundance of bacteria, and the abnormal functional predictions.


Assuntos
Neoplasias Colorretais , Microbioma Gastrointestinal , Humanos , Microbioma Gastrointestinal/genética , Disbiose/microbiologia , Fezes/microbiologia , Bactérias/genética
19.
Front Cell Infect Microbiol ; 12: 1059647, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-36389153

RESUMO

The male zooid of Antheraea pernyi (A. pernyi) accumulates several nutrients and physiological activity-related substances for reproduction. Some components in the extracts of the male zooid of A. pernyi (EMZAP) have several functions, such as protecting the liver, enhancing immunity, antiatheroscloresis, anti-aging, and antitumor effects. In this study, we investigated the ameliorating effects on high-fat diet (HFD)-induced non-alcoholic fatty liver disease (NAFLD). The EMZAP treatment could ameliorate NAFLD and effectively decrease the serum total cholesterol, triglyceride and low-density lipoprotein levels and a significant increase in serum high-density lipoprotein levels was observed. Additionally, the EMZAP treatment reduced the levels of liver-function enzymes and pro-inflammatory cytokines (i.e., IL-6, IL-8, TNF-α, TGF-ß1) and also the oxidative stress indices and regulated the expression of genes associated with fatty acid metabolism (SREBP-1c, PPARα, ACOX-1, CPT-1) in the liver to prevent the development of NAFLD. Furthermore, EMZAP enhanced the diversity and richness of the beneficial intestinal microbes, suggesting its potential as a dietary supplement and functional food to combat NAFLD induced by HFD.


Assuntos
Mariposas , Hepatopatia Gordurosa não Alcoólica , Camundongos , Masculino , Animais , Hepatopatia Gordurosa não Alcoólica/etiologia , Hepatopatia Gordurosa não Alcoólica/genética , Dieta Hiperlipídica/efeitos adversos , Disbiose , Camundongos Endogâmicos C57BL
20.
Front Cell Infect Microbiol ; 12: 1022603, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-36389160

RESUMO

Anastomotic leak (AL) is a life-threatening postoperative complication following colorectal surgery, which has not decreased over time. Until now, no specific risk factors or surgical technique could be targeted to improve anastomotic healing. In the past decade, gut microbiota dysbiosis has been recognized to contribute to AL, but the exact effects are still vague. In this context, interpretation of the mechanisms underlying how the gut microbiota contributes to AL is significant for improving patients' outcomes. This review concentrates on novel findings to explain how the gut microbiota of patients with AL are altered, how the AL-specific pathogen colonizes and is enriched on the anastomosis site, and how these pathogens conduct their tissue breakdown effects. We build up a framework between the gut microbiota and AL on three levels. Firstly, factors that shape the gut microbiota profiles in patients who developed AL after colorectal surgery include preoperative intervention and surgical factors. Secondly, AL-specific pathogenic or collagenase bacteria adhere to the intestinal mucosa and defend against host clearance, including the interaction between bacterial adhesion and host extracellular matrix (ECM), the biofilm formation, and the weakened host commercial bacterial resistance. Thirdly, we interpret the potential mechanisms of pathogen-induced poor anastomotic healing.


Assuntos
Neoplasias Colorretais , Microbioma Gastrointestinal , Humanos , Disbiose/microbiologia , Anastomose Cirúrgica/efeitos adversos , Reto/microbiologia , Fístula Anastomótica/microbiologia , Neoplasias Colorretais/complicações
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