Academic literature on the topic 'Microbiota intestinale (Gut microbiota)'
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Journal articles on the topic "Microbiota intestinale (Gut microbiota)"
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Liu, Qihong, Yunfeng Luo, and Xiao Ke. "Interaction between the Gut Microbiota and Intestinal Motility." Evidence-Based Complementary and Alternative Medicine 2022 (November 15, 2022): 1–5. http://dx.doi.org/10.1155/2022/3240573.
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The gut microbiota is the largest symbiotic ecosystem with the host and has been proven to play an important role in maintaining the stability of the intestinal environment. The imbalance of the gut microbiota is caused by the imbalance between the symbiotic microbiota and the pathogenic microbiota. The commensal microbiome regulates intestinal motility, while the pathogenic microbiome causes intestinal motility disorder, resulting in disease development. Intestinal motility is a relatively general term, and its meaning may include intestinal muscle contraction, intestinal wall biomechanics, intestinal compliance, and transmission. The role of intestinal microecology and intestinal motility are interrelated, intestinal flora disorder mediates intestinal motility, and abnormal intestinal motility affects colonization of the intestinal flora. In this review, we briefly outlined the interaction between gut microbiota and intestinal motility and provided a reference for future studies.
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Thomas, Linda V., Theo Ockhuizen, and Kaori Suzuki. "Exploring the influence of the gut microbiota and probiotics on health: a symposium report." British Journal of Nutrition 112, S1 (June 23, 2014): S1—S18. http://dx.doi.org/10.1017/s0007114514001275.
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The present report describes the presentations delivered at the 7th International Yakult Symposium, ‘The Intestinal Microbiota and Probiotics: Exploiting Their Influence on Health’, in London on 22–23 April 2013. The following two themes associated with health risks were covered: (1) the impact of age and diet on the gut microbiota and (2) the gut microbiota's interaction with the host. The strong influence of the maternal gut microbiota on neonatal colonisation was reported, as well as rapid changes in the gut microbiome of older people who move from community living to residential care. The effects of dietary changes on gut metabolism were described and the potential influence of inter-individual microbiota differences was noted, in particular the presence/absence of keystone species involved in butyrate metabolism. Several speakers highlighted the association between certain metabolic disorders and imbalanced or less diverse microbiota. Data from metagenomic analyses and novel techniques (including anex vivohuman mucosa model) provided new insights into the microbiota's influence on coeliac, obesity-related and inflammatory diseases, as well as the potential of probiotics.Akkermansia muciniphilaandFaecalibacterium prausnitziiwere suggested as targets for intervention. Host–microbiota interactions were explored in the context of gut barrier function, pathogenic bacteria recognition, and the ability of the immune system to induce either tolerogenic or inflammatory responses. There was speculation that the gut microbiota should be considered a separate organ, and whether analysis of an individual's microbiota could be useful in identifying their disease risk and/or therapy; however, more research is needed into specific diseases, different population groups and microbial interventions including probiotics.
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Meiliana, Anna, and Andi Wijaya. "Gut Microbiota, Obesity and Metabolic Dysfunction." Indonesian Biomedical Journal 3, no. 3 (December 1, 2011): 150. http://dx.doi.org/10.18585/inabj.v3i3.147.
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BACKGROUND: The prevalence of obesity and related disorders such as metabolic syndrome and diabetes has vastly increased throughout the world. Recent insights have generated an entirely new perspective suggesting that our microbiota might be involved in the development of these disorders. This represents an area of scientific need, opportunity and challenge. The insights gleaned should help to address several pressing global health problems.CONTENT: Our bowels have two major roles: the digestion and absorption of nutrients and the maintenance of a barrier against the external environment. They fulfill these functions in the context of, and with the help from, tens of trillions of resident microbes, known as the gut microbiota. Studies have demonstrated that obesity and metabolic syndrome may be associated with profound microbiotal changes, and the induction of a metabolic syndrome phenotype through fecal transplants corroborates the important role of the microbiota in this disease. Dietary composition and caloric intake appear to swiftly regulate intestinal microbial composition and function.SUMMARY: The interaction of the intestinal microbial world with its host, and its mutual regulation, will become one of the important topics of biomedical research and will provide us with further insights at the interface of microbiota, metabolism, metabolic syndrome, and obesity. A better understanding of the interaction between certain diets and the human gut microbiome should help to develop new guidelines for feeding humans at various time points in their life, help to improve global human health, and establish ways to prevent or treat various food-related diseases.KEYWORDS: gut microbiota, obesity, metabolic syndrome, type 2 diabetes
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Neophytou, Constantina, and Chrysoula Pitsouli. "How Gut Microbes Nurture Intestinal Stem Cells: A Drosophila Perspective." Metabolites 12, no. 2 (February 10, 2022): 169. http://dx.doi.org/10.3390/metabo12020169.
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Host-microbiota interactions are key modulators of host physiology and behavior. Accumulating evidence suggests that the complex interplay between microbiota, diet and the intestine controls host health. Great emphasis has been given on how gut microbes have evolved to harvest energy from the diet to control energy balance, host metabolism and fitness. In addition, many metabolites essential for intestinal homeostasis are mainly derived from gut microbiota and can alleviate nutritional imbalances. However, due to the high complexity of the system, the molecular mechanisms that control host-microbiota mutualism, as well as whether and how microbiota affects host intestinal stem cells (ISCs) remain elusive. Drosophila encompasses a low complexity intestinal microbiome and has recently emerged as a system that might uncover evolutionarily conserved mechanisms of microbiota-derived nutrient ISC regulation. Here, we review recent studies using the Drosophila model that directly link microbiota-derived metabolites and ISC function. This research field provides exciting perspectives for putative future treatments of ISC-related diseases based on monitoring and manipulating intestinal microbiota.
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Leardini, Davide, Edoardo Muratore, Daniele Zama, Arcangelo Prete, Andrea Pession, and Riccardo Masetti. "Il ruolo del microbiota intestinale nella modulazione immunitaria." Medico e Bambino pagine elettroniche 23, no. 6 (June 30, 2020): 130–36. http://dx.doi.org/10.53126/mebxxiiig130.
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The intestinal microbiota plays a crucial role in numerous physiological and pathological processes of the developmental age. The development of new investigation methods, such as next generation sequencing, has allowed a more precise characterization of the intestinal microbiota. This allowed us to deepen the complex relationship between the microbial flora and our organism. One of the many functions that emerged is the ability to modulate the host's immune system. The transplantation of hematopoietic stem cells represents a privileged setting for studying this interaction since, after the procedure, we witness the immune reconstruction starting from the donor precursors. The gut microbiota influences the development of major infectious and immune-mediated complications of transplantation and has a significant impact on patient survival. These evidences underline the possible therapeutic implications of the modulation of the intestinal microbiota. An in-depth study of the relationship between the immune system and microbiotic flora could allow us to better understand the role of the latter in other infectious or immune-mediated diseases.
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Пальцын, А. А. "Gut microbiota." ZHurnal «Patologicheskaia fiziologiia i eksperimental`naia terapiia», no. 4() (November 21, 2018): 202–8. http://dx.doi.org/10.25557/0031-2991.2018.04.202-208.
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Совершенствование методов генетического анализа и развернувшиеся на этой основе работы по международному проекту «Микробиом человека» представили большой объем знаний, существенно меняющих представления об эволюции живой природы и о механизмах развития многих болезней. Пришло осознание факта, что здоровье и болезни человека в большой степени определяются взаимодействием его собственных клеток с населяющими его тело (прежде всего кишечник) микробными (прежде всего бактериальными) клетками. Главенство в этом вопросе бактерий кишечника объясняется их подавляющей многочисленностью, позицией на первичном рубеже обмена со средой и невозможностью жизни без этого обмена. Результаты обширных теоретических и клинических исследований уже сегодня могут стать основой профилактики и терапии некоторых незаразных пандемий современности. Однако научно вполне достижимый дальнейший масштабный успех в преодолении этих пандемий тормозится внешними причинами. Кишечная микробиота связывает здоровье людей с экологией планеты, с сельским хозяйством и пищевой промышленностью. Действия же международных корпораций направляются интересами не здравоохранения, а получения максимальной выгоды в минимальные сроки. Improving methods of genetic analysis and the work developed on this basis under the «Human Microbiome» international project presented a large amount of knowledge that has significantly changed ideas about the evolution of living nature and mechanisms underlying development of many diseases. People became aware of the fact that human health and diseases are largely determined by the interaction of the body’s own cells with the microbial (primarily bacterial) cells inhabiting the body (primarily the intestine). The dominance of intestinal bacteria in this aspect is explained by their overwhelming multiplicity, position on the primary border of exchange with the environment, and the impossibility of life without this exchange. Results of extensive theoretical and clinical research already today can become a basis for prevention and treatment of some current non-infectious pandemics. However, although further, large-scale success in overcoming these pandemics is scientifically quite achievable, certain political reasons hamper it. Intestinal microbiota connects human health with the global ecology, agriculture, and the food industry while actions of governments and international corporations are driven by obtaining maximum benefits in the shortest possible time rather than interests of health care.
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Eom, Jung A., Goo Hyun Kwon, Na Yeon Kim, Eun Ju Park, Sung Min Won, Jin Ju Jeong, Ganesan Raja, et al. "Diet-Regulating Microbiota and Host Immune System in Liver Disease." International Journal of Molecular Sciences 22, no. 12 (June 13, 2021): 6326. http://dx.doi.org/10.3390/ijms22126326.
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The gut microbiota has been known to modulate the immune responses in chronic liver diseases. Recent evidence suggests that effects of dietary foods on health care and human diseases are related to both the immune reaction and the microbiome. The gut-microbiome and intestinal immune system play a central role in the control of bacterial translocation-induced liver disease. Dysbiosis, small intestinal bacterial overgrowth, translocation, endotoxemia, and the direct effects of metabolites are the main events in the gut-liver axis, and immune responses act on every pathways of chronic liver disease. Microbiome-derived metabolites or bacteria themselves regulate immune cell functions such as recognition or activation of receptors, the control of gene expression by epigenetic change, activation of immune cells, and the integration of cellular metabolism. Here, we reviewed recent reports about the immunologic role of gut microbiotas in liver disease, highlighting the role of diet in chronic liver disease.
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Janczy, Agata, Magdalena Landowska, and Zdzisław Kochan. "Gut microbiome dysbiosis in anorexia nervosa." Postępy Higieny i Medycyny Doświadczalnej 75 (April 29, 2021): 283–91. http://dx.doi.org/10.5604/01.3001.0014.8601.
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Anorexia nervosa (AN) is described as an eating disorder, which is characterized by malnutrition, a fear of gaining body mass, and a disturbed self-body image. This disease is dependent on biological, psychological and socio-cultural factors. Among the various biological factors, the importance of intestinal microbiota has recently attracted much attention. Identification of the gut microbiota dysbiosis in patients with AN has opened new and promising research directions. Recent observations focus in particular on the association between intestinal microorganisms and the occurrence of functional gastrointestinal disorders associated with anorexia, anxiety and depression, as well as the regulation of eating habits. The composition of the gut microbiota differs between patients with AN and individuals with normal body mass. This is due to the incorrect diet of patients; on the other hand, there is growing interest in the role of intestinal microbiota in the pathogenesis of AN, its changes through re-nutrition practices, and in particular the modulation of intestinal microbiological composition by means of nutritional interventions or the use of preand probiotics as standard supplements therapy of eating disorders. There is a need for further research about the microbiome - intestine - brain axis. Furthermore, consequences of changes in dietary habits as part of AN treatment are also unknown. However, better knowledge about the relationship between the gut microbiome and the brain can help improve the treatment of this disorder. This review aims to present the current knowledge about the potential role of intestinal microbiota in the pathogenesis, course and treatment of AN.
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Chernevskaya, E. A., and N. V. Beloborodova. "Gut Microbiome in Critical Illness (Review)." General Reanimatology 14, no. 5 (October 28, 2018): 96–119. http://dx.doi.org/10.15360/1813-9779-2018-5-96-119.
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Radical changes in the composition, diversity and metabolic activity of gut microbiome in critically ill patients most probably affect adversely the outcome of treatment. Microbiota dysfunction may be a predictor and presumably the main cause of infectious complications and sepsis. Clinicists use objective scales for evaluation of patient condition severity including specific parameters of disorders of organs and systems; however, microbiota function is not considered specific and, hence, not evaluated. Technical capabilities of the recent decade have allowed characterizing the intestinal microbiota and that helped understanding the ongoing processes. The authors have analyzed data about the role of intestinal microbiota as a metabolic 'reactor' during critical states, possible complications related to misbalance of 'harmful' and 'beneficial' bacteria, and examined potential of a targeted therapy aimed directly at correction of intestinal microbiota. Search for papers was carried out using Scopus and Web of Science databases 2001 to 2018 years: (Gut Microbiota) AND (Critically ill OR Intensive care unit), key words taken for the search were: intestinal microbiota, metabolism, sepsis, antibiotics, critically ill patients, multiple organ failure. A number of questions in understanding of the interaction between gut microbiome and host remain open. It is necessary to take into account interference of microbial metabolism while assessing metabolome of patients with sepsis. Among low-molecular compounds found in blood of sepsis patients, special attention should be paid to molecules that can be classified as ‘common metabolites’ of humans and bacteria, for example, degradation products of aromatic compounds, which many-fold rise in blood of septic patients. It is necessary to take into consideration and experimentally model changes in the human internal environment, which occur during radical transformation of microbiome in critically ill patients. Such approach brings in new prospects for objective monitoring of diseases by evaluating metabolic profile at a particular moment of time based on integral indices reflecting the status of microbiome/metabolome system, which will supply new targets for therapeutic intervention in future.
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Garrett, Wendy S. "Gut Microbiota and Intestinal Inflammation." Blood 120, no. 21 (November 16, 2012): SCI—49—SCI—49. http://dx.doi.org/10.1182/blood.v120.21.sci-49.sci-49.
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Abstract Abstract SCI-49 Numerous studies of the microbiota that are found throughout the human body are under way, with the goal of unraveling the role of microbes in human physiology. Using experimental colitis models, we are investigating microbes that may instigate chronic inflammation, and we are studying putative beneficial microbes whose reduced presence may impact not only host response to the microbiota but also the behavior of the endogenous microbiota. Genomic approaches, combined with following microbial community response to a spectrum of dietary and pharmacologic perturbations, are shedding light on the dynamic operations of the microbiota that influence health and disease. Chronic inflammation in the intestine is not only the central pathophysiologic mechanism of inflammatory bowel disease (IBD) but also a key contributor to colorectal cancer. Ongoing work on the colorectal microbiome, using experimental models and human tumors, will be discussed. Collectively, our studies support the utility of wedding culture-independent and culture-dependent studies with mouse models for defining how the gut microbiota works in concert with the mucosal immune system to shape disease susceptibility for IBD and colorectal cancer. Disclosures: Garrett: Groupe Danone: Research Funding.
Dissertations / Theses on the topic "Microbiota intestinale (Gut microbiota)"
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Bilen, Melhem. "Description of the human gut microbiota by culturomics." Thesis, Aix-Marseille, 2018. http://www.theses.fr/2018AIXM0177/document.
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Le microbiote intestinal humain a été fortement corrélé avec la santé humaine et les maladies et a montré un potentiel dans les développements thérapeutiques. La métagénomique a déjà montré qu'elle était capable de générer beaucoup de données, dont certaines sont dénuées de sens et constituaient la "matière noire". Alors culturomics a été développée pour compléter la métagénomique en ciblant des espèces bactériennes précédemment non cultivées. En utilisant la culturomics, nous avons décrit le microbiote intestinal humain des Pygmées et réussi à isoler un nombre significatif d'espèces bactériennes parmi lesquelles 38 étaient de nouvelles espèces. En comparant les résultats métagénomiques aux données culturomics, on constate que seulement 26% des espèces isolées ont été récupérées par métagénomique et que jusqu'à 59% des Operational taxonomic units détectées correspondaient à de nouvelles espèces bactériennes isolées par culturomique dans cette étude ou dans les précédentesThe human gut microbiota has been correlated in general health and diseases. Thus its description became mandatory to better understand its role and therapeutic potential. However, metagenomics has previously showed to be able to generate a lot of data, of which some are meaningless and constituted the “Dark matter”. Thus, culturomics was developed to complement metagenomics by targeting previously uncultured bacterial species. Using culturomics, we described the human gut microbiota of Pygmy people and succeeded in isolating a significant number of bacterial species out of which 38 were new species. Comparing metagenomics results to culturomics data, we see that only 26% of the isolated species were recovered by metagenomics and that up to 59% of the Operational taxonomic units detected corresponded to new bacterial species isolated by culturomics either in this study or in previous ones
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Duca, Frank. "Altered satiation signaling in obesity : the role of nutrients, gut peptides, and gut microbiota." Paris 6, 2013. http://www.theses.fr/2013PA066078.
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Food intake is controlled by a highly complex and distributed neural system integrating many sensory inputs, most notably those arising from the gastrointestinal tract in response to a meal. Reduced sensitivity to intestinal nutrients has been proposed to be partly responsible for increased energy intake and weight gain in both animals and humans during HF feeding. However, the mechanism by which a HF diet impinges on post-ingestive intestinal feedback to promote overconsumption is unclear, as is the role of diminished satiation signaling in the development of obesity. Therefore, the work of this thesis attempts to discern the role of HF feeding in nutrient-induced satiation, by addressing the impact of GI peptides and the gut microbiota in diet-induced obesity in animals prone or resistant to obesity. In the first set of experiments, we found that diet-induced obese rats exhibited a reduced responsiveness to the suppressive effects of intragastric lipid loads, compared to diet-resistant rats. This was associated with altered intestinal gut peptides and GPRs, plausibly contributing to reduced lipid-induced satiation. In the next set of experiments, we showed that OP rats develop impaired GLP-1 signaling during maintenance on a HF diet. During chow feeding, OP and OR rats had similar sensitivity to the anorectic effects of GLP-1R agonism; however, HF feeding abolished the suppressive response to exendin-4 in OP rats. This was associated with downregulation of GLP-1R in the nodose ganglia, in addition to decreased circulating GLP-1 and L-cell counts. The last set of experiments demonstrates the influence of the gut microbiota in regulating intestinal chemosensory machinery and potentially promoting adiposity in OP rats. First, GF mice exhibited increased consumption for lipid solutions with associative decreases in intestinal satiation signals and fatty acid receptors, indicating that lack of microbiota reduces post-ingestive signaling to promote overeating. Next, we found that OP rats harbor a distinct microbiota profile compared to OR rats during HF feeding. By conventionalizing GF mice with OP microbiota, we replicated the obese phenotype, and associated reductions in peripheral and central appetite-related pathways. In summary, this thesis provides evidence that the interaction of a polygenetic susceptibility to obesity coupled with HF feeding reduces sensitivity to intestinal nutrients, by altering secretion and sensitivity to satiation signals that ultimately contributing to weight gain and adiposity. Additionally, further elucidation on the ability of an aberrant gut microbiota to influence regulatory systems involved in energy regulation could provide useful information for the development of therapeutic treatments for obesityLa prise alimentaire est contrôlée par un système complexe associant des modifications du système nerveux. Ces dysfonctionnents impliquent les outils de perception, notamment ceux en provenance de l'appareil gastro-intestinal en réponse à un repas. La diminution de la sensibilité intestinale aux nutriments a été décrite en partie comme responsable de l'apport énergétique accrue et du gain de poids chez les animaux et les humains au cours d'un régime hypercalorique. Cependant, le mécanisme par lequel un régime obesogène affecte les signaux intestinaux postprandiaux favorisant la surconsommation et leurs rôles dans la diminution du signal de satiété contribuant au développent de l'obésité reste très peu étayer. Par conséquent, le travail de cette thèse a pour but de caractériser le rôle d'un régime hypercalorique dans la diminution de la satiété induite par les nutriments, d'étudier le rôle des peptides gastro-intestinaux et de microbiote au cours d'un régime hypercalorique favorisant l'obésité chez les rats OP. Dans la première série d'expériences, nous avons constaté que les rats soumises un régime hypercalorique présentaient une réponse réduite aux effets suppresseurs de charges lipidiques gastriques comparé à des rats résistants à l'obésité (OR). Cette réponse a été associée à une altération des peptides intestinaux et des GPRS contribuant à une réduction du signal du satiété. Dans une deuxième série d'expériences, nous avons démontré que les rats obeses prônes (OP) développent une déficience de la voie de signalisation de GLP-1 au cours d'un régime hypercalorique. Sous un régime normal, les rats OP et OR avaient la même sensibilité aux effets anorexigène d'un agoniste du récepteur du GLP-1. Toutefois, le régime obesogène abolit la réponse suppressive de l'exendin-4 chez des rats OP. Ceci a été associée à une régulation négative de l'expression du GLP-1R dans les ganglions nodaux, une diminution des taux du GLP-1 circulants et du nombre des cellules L sécrétrices du GLP-1. La dernière série d'expériences démontre l'influence du microbiote intestinal dans la régulation de la chemosensibilité intestinale favorisant l'adiposité chez les rats OP. Les souris axéniques présentent une consommation accrue de solutions lipidiques associé à une diminution du signal satiétogène intestinal et des récepteurs d'acides gras. Nous avons conclu que l'absence du microbiote réduit le signal de satiété postprandial contribuant à la surconsommation des nutriments. Par la suite, nous avons identifié que les rats OP possèdent un profil du microbiote intestinal distinct de rats OR sous un régime hypercalorique. La conventionnalisation des souris axéniques avec le microbiote issu des rats OP, reproduit parfaitement le phénotype obèse avec à une réduction de la signalisation centrale et périphérique des voies contrôlant la prise alimentaire. En résumé, cette thèse apporte la preuve que l'interaction entre une prédisposition à l'obésité généralement polygénique couplée à une alimentation obesogène réduit la sensibilité intestinale aux nutriments, altérant la sécrétion et la sensibilité aux signaux de satiété. Ces effets ont pour conséquence un gain de poids et une expansion de la masse grasse. De plus, des preuves scientifiques supplémentaires sur la capacité d'un microbiote intestinal aberrant d'influencer les systèmes de régulation impliqués dans le maintien de l'homéostasie énergétique pourraient fournir des informations scientifiquement fondées afin de prévenir le développement et l'installation de l'obésité et contribuer aux progrès thérapeutiques de l'obésité
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Engevik, Melinda A. "Ion Transport and the Gut Microbiota." University of Cincinnati / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1397466973.
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ANCONA, GIUSEPPE. "ROLE OF CART ON GUT MICROBIAL DYSBIOSIS, STUDYING THE GUT/BLOOD MICROBIOTA DURING THE FIRST TWO YEARS OF SUPPRESSIVE CART." Doctoral thesis, Università degli Studi di Milano, 2019. http://hdl.handle.net/2434/628966.
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ROLE OF CART ON GUT MICROBIAL DYSBIOSIS, STUDYING THE GUT/BLOOD MICROBIOTA DURING THE FIRST TWO YEARS OF SUPPRESSIVE CART
BACKGROUND Microbial dysbiosis features HIV+ individuals, both naïve and cART-treated, and is linked to anatomical/structural changes in the gastrointestinal (GI) tract, leading to microbial translocation (MT) and immune activation. Given that data on microbiota modifications during long-term therapy are lacking, we investigated gut/blood microbiota during the first 2 years of suppressive cART.
METHODS We enrolled 138 HIV+ subjects. Plasma was collected at baseline (T0) and following 12 (T12) and 24 months (T24) of cART. CD8+ T-cell activation (CD38+; CD38+CD45R0+), MT (sCD14 and EndocAb) and GI damage (IFAB-P) were studied. In a sub-group of 41 patients (pts) we also evaluated GI permeability (urinary LAC/MAN test), inflammation (faecal calprotectin), 16SDNA (MT marker) and gut persistence score, metagenomic function analysis (Picrust) as well as peripheral and faecal microbiota (DNA extraction and 16S Metagenomic Sequencing; MiSeq Illumina®). For the microbiota analyses we enrolled 15 HIV- subjects as controls. All groups were analysed by Wilcoxon test, Kruskal-Wallis test and Permanova analysis.
RESULTS 88% were male, 65% MSM, 6% HCV+; median age, CD4+ count, HIV RNA and duration of infection were respectively 38 years, 312/mmc, 5.03 log10cp/mL and 11.5 months. Following cART we registered a reduction of activated and activated/memory CD+8 T-cells (both with p<0.0001), an increase of EndoCab levels (p<0.0001) yet no significant changes in plasma sCD14. In contrast, an increase of I-FABP (p<0.0001) vis- à -vis a reduction of LAC/MAN test (p=0.03) and faecal calprotectin (p=0.01) were found.
In faeces, cART resulted in a limited modification of the relative abundance of the microbiota, however differences between pts and controls were detected in the Firmicutes, Bacteroidetes and Actynobacteria phyla. Alpha-diversity showed higher richness in HIV+ vs controls (observed: p=0.006; Chao1: p=0.002) and these differences were maintained at T12 and T24. PCoA plot analyses showed a trend to the separation of pts and controls at all time-points yet the latter overlapped regardless of treatment status and length of cART. Lefse analyses (LDS >2.0) in HIV+ showed a significant increase of Veillonellaceae at T12 (p=0.007) and T24 (p=0.001) Desulfovibrionaceae at T24 (p=0.022) and Prevotellaceae at T24 (p=0.018). Further, many differences between pts and controls was detected in HIV+ .
This persistent dysbiosis was associated with the continuous mucosal damage, despite cART introduction: I-FABP were positively correlated with Veillonellaceae both at T12 (r2=0.197; p=0.030;) and T24 (r2=0.156; p=0.017). Interestingly, when we stratified patients according to cART regimens, we found that only NNRTI-based therapy significantly reduced richness (observed: p=0.038; Chao1: p=0.006), but not evenness indexes over time. Furthermore, the relative abundance analyses showed a different profile at both family and genus levels, with NNRTI-based regimens significantly reducing the families of Coriobacteriaceae, Peptococcaceae and increasing the Veillonellaceae family. On the opposite, INSTI-based regimens resulted in decreased Peptococcaceae and increased Veillonellaceae families, as well as in higher Allisonella genus. No major effects following PI-based regimens were detected; no modifications about gut persistence score analysis as well as predicted functional metagenomic pathway analysis were found.
Plasma microbiota analyses revealed no major changes of relative abundance parameters during cART and in comparison with uninfected controls. Decreased alpha-diversity was nonetheless found in HIV+ compared to controls (Shannon: p=0.02, Simpson: p=0.009) and persisted both at T12 and T24.
CONCLUSIONS HIV-related modifications of the microbiota occur within the GI tract and not in the blood and are minimally affected by long-term effective cART, despite evidence of the containment of gut inflammation. These data suggest the ability of the virus to irreversibly impact the microbiological core of chronically-infected individuals.
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Nyangahu, Donald D. "Alterations in preconception, antenatal, and postnatal maternal gut microbiota influence offspring intestinal microbiota and immunity." Doctoral thesis, University of Cape Town, 2017. http://hdl.handle.net/11427/25479.
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Maternal microbiota during pregnancy, as well as maternal disease state, may impact offspring gut bacterial colonisation. Here, we explore the impact of maternal antibiotics during gestation and/or nursing on offspring gut microbiota. Further, we investigate the effect of preconception helminth infections on maternal and infant gut microbiota. For maternal antibiotic experiments, dams were fed vancomycin, polymyxin B, or both, in drinking water during gestation, nursing or gestation plus nursing, and their offspring microbiota analysed at 14 days of life, alongside immunity in the spleens. Offspring born to vancomycin treated mothers had significantly higher relative abundance of Proteobacteria and Tenericutes while maternal oral polymyxin B led to significantly lower abundance of Proteobacteria and Deferribacteres in infants. Maternal oral vancomycin led to significant reduction in proportions of infant central memory CD4+ T cells (CD4+CD44hiCD62Lhi) regardless of antibiotic timing. Effector memory CD4+ T cells were significantly lower in pups born to dams treated with polymyxin B while nursing while proportions of central memory CD4 T cells were significantly increased in gestation only or gestation plus nursing pups. In addition, oral vancomycin in dams during nursing resulted in significantly reduced proportions of both total and follicular B cells in offspring born to antibiotic treated dams. Pups born to Vancomycin treated mothers had a significant delay in growth when infected with Respiratory Syncytial Virus (RSV). On the other hand, pups born to mothers treated with Polymyxin B during gestation or gestation plus nursing were susceptible to Nippostrongylus brasiliensis (Nb) infection. In the second study, we infected female BALB/c mice with 500Nb L3 three weeks prior to mating and examined the effect of preconception helminth infection on offspring microbiota and immunity. Preconception Nb infections led to alterations of maternal gut microbiota during pregnancy. In addition, we observed dramatic differences in offspring microbiota in pups born to previously helminth infected dams. Coriobacteriaceae were predominant in pups born to previously Nb infected dams when compared to uninfected dams. Overall, manipulation of maternal microbiota during gestation or lactation profoundly impacts offspring growth, intestinal microbiota and immunity to RSV and helminths.
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Bassignani, Ariane. "Metaproteomics analysis to study functionalities of the gut microbiota in large cohorts." Electronic Thesis or Diss., Sorbonne université, 2019. https://theses.hal.science/tel-02871891.
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La métaprotéomique s’attache à identifier et quantifier les protéines d’échantillons biologiques complexes comme le microbiote intestinal humain. L’analyse de plusieurs centaines d’échantillons revêt un intérêt évident compte tenu de la reconnaissance croissante de cet écosystème en tant que partenaire santé. Cependant, les méthodes et protocoles utilisés jusqu’à ce jour en métaprotéomique ne sont pas adaptés à des études de grande ampleur. Nous avons développé des algorithmes, évalué et comparé plusieurs approches d’identification des peptides et protéines et proposé des critères d’évaluation systématiques, avec un intérêt particulier porté sur la réplicabilité des identifications, afin de développer un pipeline de prétraitement adapté à des études d’envergure. Ce travail apporte un socle méthodologique jusqu’ici manquant dans le domaine de la métaprotéomique du microbiote intestinal humain. Nous avons également comparé des méthodes de normalisation des XIC et développé une méthodologie d’imputation des données manquantes permettant d’affiner les estimations d’abondances obtenues par la méthode de SC. Ce travail de thèse a permis de mettre en évidence des biomarqueurs microbiens potentiellement d’intérêt pour prédire la réponse à un régime amaigrissant ou pour caractériser différents phénotypes de MICI. Nous avons également analysé le métaprotéome de plus de 200 patients dans le cadre de l’ANR ProteoCardis adossée au projet MetaCardis, et s’intéressant au lien possible entre microbiote intestinal et maladies cardiovasculaires. La recherche de protéines d’intérêt parmi ces données devrait permettre de découvrir des candidats biomarqueurs de maladies cardiovasculairesMetaproteomics focuses on identifying and quantifying proteins in complex biological samples such as the human gut microbiota. The analysis of several hundred of samples is of interest given the growing recognition of this ecosystem as a health partner. However, the methods and protocols used so far in metaproteomics are not suitable for large-scale studies. We have therefore developed algorithms, evaluated and compared several identification approaches for peptides and proteins and proposed systematic evaluation criteria, with a particular interest in the replicability of identifications, in order to develop a pre-treatment pipeline suitable for wide-ranging studies. This work bring a methodological base so far missing in the field of the metaproteomics of the human gut microbiota. Quantification of peptides and proteins by XIC has never been performed on this type of data, we have also compared normalization methods and developed a methodology for imputing missing data to refine the abundance estimations obtained by the more classical method of SC. This thesis work has highlighted microbial biomarkers of potential interest for predicting the response to a slimming diet, or to characterize various phenotypes of IBD. We have also been able to analyse the metaproteome of more than 200 patients in the framework of the ProteoCardis ANR, which is ancillary to the European project MetaCardis, and which focuses on the potential link between gut microbiota and cardiovascular diseases. The search for proteins of interest among these data should allow us to discover protective or aggravating candidate biomarkers of cardiovascular diseases
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Nicolas, Simon. "Modulation de l'homéostasie glucidique par transfert de microbiote intestinal chez la souris conventionnelle." Thesis, Toulouse 3, 2016. http://www.theses.fr/2016TOU30176/document.
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De nos jours, le changement de style de vie et la consommation excessive d'aliments riches en énergie sont associés avec l'augmentation majeure de l'incidence des maladies métaboliques comme l'obésité et le diabète de type 2. Le diabète de type 2 est caractérisé, entre autre, par une augmentation de la production hépatique de glucose responsable d'une hyperglycémie chronique. Durant ces 10 dernières années, plusieurs études ont suggéré que le microbiote intestinal pouvait être impliqué dans le développement des maladies métaboliques. Le microbiote intestinal est composé de plusieurs milliards de bactéries réparties en plus de 1000 espèces différentes qui colonisent le tractus digestif. Plusieurs études ont montré que certaines pathologies comme le diabète et l'obésité sont caractérisées par des altérations taxonomiques et fonctionnelles du microbiote intestinal. De plus, la colonisation de souris axéniques (i.e. dépourvues de microbiote) par un microbiote intestinal provenant de souris ou d'Hommes obèses/diabétiques est suffisante pour induire la pathologie. Ces résultats suggèrent que les modifications du microbiote intestinal retrouvées chez les patients obèses/diabétiques sont potentiellement impliquées dans le développement des maladies métaboliques. Cependant, l'absence de microbiote intestinal chez les souris axéniques induit des altérations structurelles et fonctionnelles de l'intestin comme une hyperperméabilité intestinale ou un système immunitaire atrophié. Dans ces conditions, il est possible de se demander si les effets délétères induits par la colonisation des souris axéniques avec un microbiote modifié peuvent être observés chez des souris conventionnelles. Pour répondre à cette question nous avons développé un nouveau protocole de transfert de microbiote intestinal dans un modèle de souris conventionnelles. Nous avons transféré le microbiote contenu dans le caecum de souris obèses (" microbiote obèse ") et celui contenu dans le caecum de souris minces (" microbiote mince ") dans des souris conventionnelles non traitées aux antibiotiques. De manière surprenante, le transfert du " microbiote obèse " a induit une diminution de la glycémie à jeun associée à une baisse de la néoglucogenèse hépatique chez les souris transplantées. A l'inverse, le transfert du " microbiote mince " n'a pas modifié la néoglucogenèse. De plus, le transfert du " microbiote obèse " a induit des modifications taxonomiques et fonctionnelles du microbiote intestinal des souris transplantées. De manière intéressante, une fois nourries avec un régime hyperlipidique les souris ayant reçu le " microbiote obèse " ont conservé une glycémie à jeun plus faible que les souris non transplantées. Encore une fois, ce phénotype résulte d'une diminution de la production hépatique de glucose caractérisée par une baisse de l'activité des enzymes néoglucogéniques phosphoenolpyruvate carboxykinase et glucose-6-phosphatase. Par ailleurs, ces souris sont également moins grasses que les souris non transplantées. En conclusion, nous avons montré que le transfert d'un " microbiote obèse " peut moduler le métabolisme hépatique et prévenir l'augmentation de la néoglucogenèse hépatique normalement induite par le régime hyperlipidique chez des souris conventionnelles. Ces travaux de thèse ont montré d'une part, que la modification du microbiote intestinal de souris conventionnelles est possible par transfert de microbiote caecal. D'autre part et contre toutes attentes, ces résultats mettent en lumière que, contrairement aux observations faites chez les souris axéniques, le transfert d'un " microbiote obèse " dans une souris conventionnelle n'induit pas les phénotypes caractéristiques des maladies métaboliques. Par ailleurs, ce modèle de transfert caecal pourrait être utile pour la compréhension du rôle des bactéries intestinales sur le développement des maladies métaboliquesNowadays, the change of lifestyle and increase in the consumption of high-calorie foods are associated with a marked rise of the prevalence of metabolic diseases, including obesity and type 2 diabetes. Type 2 diabetes is linked, at least in part, to an increase of hepatic glucose production responsible for a fasting hyperglycemia. In the past decade, an increasing body of evidence has proposed gut microbiota as a new factor contributing to these metabolic alterations. Gut microbiota consists of trillions of bacteria identifying more than 1000 different species that inhabit our intestine. A body of work has demonstrated that multiple pathologies such as type 2 diabetes and obesity are characterized by an altered proportion and activity of the gut microbiota. In addition, the colonization of germ-free mice with the gut microbiota from either obese/diabetic humans or obese/diabetic mice transfers the phenotype. These results suggest that the modifications of the gut microbiota found in obese/diabetic patients are a potential etiologic factor for those diseases. Nevertheless, the lack of microbiota in germ-free mice determines both structural and functional alterations such as gut hyperpermeability and the atrophy of the immune system. Therefore, we could wonder whether the detrimental effects of the gut microbiota from obese/diabetic patients observed in germ-free mice may also be observed in healthy conventional mice. To address this issue, we have developed a new gut microbiota transferring process from conventional mice to other mice. We have transferred the cecal microbiota harvested from either obese ("obese microbiota") or lean ("lean microbiota") mice in antibiotic-free conventional mice. Surprisingly, the mice which received the "obese microbiota" had a reduced fasted glycaemia compared to the mice which received the "lean microbiota". This diminution could be attributed to a decrease of the hepatic gluconeogenesis since conversion from pyruvate to glucose and phosphoenolpyruvate carboxykinase activity were lower in the liver of mice which received the "obese microbiota". Conversely, the transfer of the "lean microbiota" did not affect the hepatic gluconeogenesis. In addition, the transfer of the "obese microbiota" changed gut microbiota composition and the microbiome of recipient mice. Interestingly, mice which received the "obese microbiota" and fed a high-fat diet still exhibited reduced fed and fasted glycaemia. Once again, this phenotype was due to a decrease of hepatic gluconeogenesis characterized by a diminution of phosphoenolpyruvate carboxykinase and glucose-6-phosphatase activity. In addition, the mice which received the "obese microbiota" had less adiposity compared to the non-transferred mice. Finally, we reported that transferring the "obese microbiota" impact on hepatic metabolism and prevent HFD-increase hepatic gluconeogenesis. On the one hand, these thesis works, have demonstrated that it is possible to modify the gut microbiota by our caecal transferring process. On the other hand, our results suggest that the transfer of the "obese microbiota" in conventional mice does not induced some characteristics of metabolic diseases contrary to that it is observed in germ-free mice. Furthermore, this kind of gut microbiota transferring process may be useful for a better understanding of the etiology of metabolic diseases
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Patrascu, Isabelle. "Description des systèmes enzymatiques du microbiote iléal humain associés à la dégradation des fibres alimentaires et exploration du microbiote fécal d'un individu obèse : approche de métagénomique fonctionnelle et recherche de glycoside hydrolases inédites." Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS098.
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La fermentation des fibres alimentaires est l’une des fonctions majeures du microbiote intestinal humain. Les bactéries fibrolytiques synthétisent un grand nombre d’enzymes, appelées Glycoside Hydrolases (GH), indispensables à la déconstruction de la grande variété structurelle des polysaccharides pariétaux que nous ingérons. Au cours de ce travail, nous avons exploré, grâce à une approche de métagénomique fonctionnelle, l’organisation et les propriétés des systèmes enzymatiques bactériens impliqués dans la dégradation des glycanes de parois végétales dans l’intestin humain.En premier lieu, nous avons cherché à déterminer si les bactéries de la muqueuse iléale étaient capables de dégrader les fibres pariétales dans un contexte sain. Cette fonction étant généralement décrite pour le microbiote colique par extrapolation de travaux menés à partir de selles humaines, nos connaissances de la dégradation des fibres dans la partie haute du tractus digestif sont donc très limitées. Un total de 20 000 clones issus du métagénome bactérien d’une partie saine de la muqueuse iléale d’un individu a été criblé pour des activités de dégradation de la carboxymethylcellulose et du xylane, deux substrats modèles des polysaccharides pariétaux. Douze clones métagénomiques positifs nous ont permis de mettre en évidence un arsenal de gènes bactériens codant pour des GH et d’autres protéines impliquées dans le métabolisme des fibres alimentaires dont certains organisés en PUL (Polysaccharide Utilization Loci), des clusters de gènes spécialisés dans la dégradation des polysaccharides complexes. Ces gènes proviennent de chromosomes bactériens assignés au genre Bacteroides ou à des espèces de Clostridiales, et codent pour des enzymes capables de dégrader également des β-glucanes à liaisons mixtes. L’étude de la prévalence de ces gènes dans les métagénomes de référence indique que plusieurs d’entre eux proviendraient de souches bactériennes plutôt spécifiques de la muqueuse iléale. De plus, certaines enzymes présentent des propriétés inédites potentiellement intéressantes dans le domaine biotechnologique. Nos recherches ont donc permis de revisiter la fonction fibrolytique du microbiote intestinal chez l’Homme et de proposer une localisation de cette fonction dès l’intestin grêle.Dans un second temps, en utilisant une approche méthodologique similaire, nous avons étudié la capacité du microbiote fécal d’un individu obèse à dégrader des polysaccharides pariétaux complexes, en général moins consommés par les individus obèses. Au total, nous avons identifié 50 clones appartenant à 14 espèces bactériennes des phyla suivants : Bacteroidetes, Firmicutes et Actinobacteria. Les inserts métagénomiques portent des gènes codant pour différentes familles de GH, impliquées dans la dégradation des polysaccharides d’intérêt. Les premières analyses de la prévalence de ces gènes chez plus d’une centaine d’individus (obèses ou non), par interrogations des catalogues de gènes microbiens de référence, suggèrent des associations avec le statut phénotypique « obèse »Among the crucial functions of the intestinal microbiota, extracting energy from food such as dietary fibres is of major importance. Facing the huge diversity of incoming complex carbohydrates, the fibrolytic bacteria synthesize a set of diversified Carbohydrate-Active Enzymes (CAZymes) including Glycoside Hydrolases (GH) that specifically disrupt complex polysaccharides. Here, using functional metagenomic approaches, we explored the organization and properties of bacterial enzymatic systems involved in the breakdown of plant cell wall (PCW) glycans in the intestinal tract.Firstly, we investigated the capacity of the microbiota associated to the human ileum mucosa to degrade complex non-starch polysaccharides in a healthy context. This function has never been investigated in this part of the intestine, but it has been rather associated to microorganisms inhabiting the colon, due to more accessible fecal samples. Using a fosmid library derived from a healthy part of the human ileal mucosa, we screened 20,000 metagenomic clones for their activities against carboxymethylcellulose and xylan chosen as models of the major PCW polysaccharides from dietary fibres. Twelve positive clones revealed a broad range of CAZyme encoding genes from Bacteroides to Clostridiales species, as well as Polysaccharide Utilization Loci (PUL). Functional GH genes were identified and break-down products examined from different polysaccharides including mixed-linkage β-glucans. Revealed CAZymes and PUL were also examined for their prevalence in human gut microbiomes. Part of them belongs to unidentified strains rather specifically established in the ileum. Others were enzymes unclassified in identified GH families or with original properties addressing novel candidates for biotechnological applications. Thus, we evidenced for the first time that the ileal mucosa associated-microbiota encompasses the enzymatic potential for PCW complex polysaccharide degradation that might start in the small intestine.In a second time, by using the same methodology, we harvested the enzymatic capacities of the fecal microbiota from an obese person to disrupt complex polysaccharides from dietary fibres usually consumed in lower quantity in obese people. This study aimed at examining the links between genes encoding enzymes specifically dedicated to PCW complex carbohydrates and the obese phenotypic status using reference microbial gene catalogs. We screened a fecal metagenomic library from an obese individual on representative PCW substrates and identified 50 clones belonging to 14 different species from the Bacteroidetes, Firmicutes and Actinobacteria phyla. The metagenomic inserts harbor genes encoding enzymes from GH families specific from complex carbohydrate degradation. First querying of the prevalence of these genes in hundreds individuals (obese and control), using catalogs of reference microbial genes, suggest associations with the "obese" phenotypic status
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Duarte, Ana Lúcia Miranda. "Changes in the feline gut microbiota associated to Toxocara cati infections." Master's thesis, Universidade de Lisboa, Faculdade de Medicina Veterinária, 2018. http://hdl.handle.net/10400.5/15794.
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Dissertação de Mestrado Integrado em Medicina VeterináriaInvestigations of the relationships between the gut microbiota and gastrointestinal parasitic nematodes are attracting growing interest by the scientific community. These studies have however been carried out mainly in humans and experimental animals, while knowledge of the make-up of the gut commensal microbiota in presence or absence of infection by parasitic nematodes in domestic animals is limited. In this study, we investigate the qualitative and quantitative impact that infections by a widespread parasite of cats (i.e. Toxocara cati) exert on the gut microbiota of feline hosts. The faecal microbiota of cats with patent infection by T. cati (= Tc+), as well as that of negative controls (= Tc-) was examined via high-throughput sequencing of the V3-V4 hypervariable region of the bacterial 16S rRNA gene, followed by bioinformatics and biostatistical analyses of sequence data. A total of 2,325,366 useable high-quality sequences were generated from the faecal samples analysed in this study and subjected to further bioinformatics analyses, which led to the identification of 128 OTUs and nine bacterial phyla, respectively. The phylum Firmicutes was predominant in all samples analysed (mean of 53.0%), followed by the phyla Proteobacteria (13.8%), Actinobacteria (13.7%) and Bacteroidetes (10.1%). Among others, bacteria of the order Lactobacillales, the family Enterococcaceae and genera Enterococcus and Dorea showed a trend towards increased abundance in Tc+ compared with Tc- samples, while no significant differences in OTU richness and diversity were recorded between Tc+ and Tcsamples (P = 0.485 and P = 0.581, respectively). However, Canonical Correlation and Redundancy Analyses were able to separate samples by infection status (P = 0.030 and P = 0.015, respectively), which suggests a correlation between the latter and the composition of the feline faecal microbiota.
RESUMO - Alterações na microbiota intestinal felina associadas a infecções por Toxocara cati - A investigação das interações entre a microbiota intestinal e os nematodes intestinais tem vindo a atrair o interesse da comunidade cientifica. No entanto, a maioria destes estudos tem sido desenvolvida em humanos e animais de laboratório, e deste modo o conhecimento da composição da microbiota comensal do intestino na presença de nematodes intestinais é reduzido. Neste estudo, foi investigado o impacto qualitativo e quantitativo da infeção pelo parasita comum dos gatos (i.e. Toxocara cati) na microbiota intestinal do hospedeiro felino. A microbiota fecal de gatos com infeção patente por T. cati (Tc+), bem como controlos negativos (Tc-) foi avaliada através de sequenciação de alto débito da região hiper-variável V3-V4 do gene 16S, seguido de análise bioinformática e bioestatística. Das amostras fecais incluídas no estudo foram obtidas um total de 2 325 366 sequências de alta qualidade e sujeitas a analise bioinformática, o que levou à identificação de 128 OTUs e nove filos bacterianos. O filo Firmicutes foi encontrado em predominância em todas as amostras (média de 53,0%), seguido do filo Proteobacteria (13,8%), Actinobacteria (13,7%) e por fim Bacteroidetes (10,1%). A abundância de determinados grupos de bactérias tendeu a aumentar nas amostras Tc+ quando comparadas com as amostras Tc-, tais como a ordem Lactobacillales, a família Enterococaceae e o género Enterococcus e Dorea. No entanto, a riqueza e diversidade das OTUs não apresentou diferenças significativas entre as amostras Tc+ e Tc- (P=0,485 e P=0,581, respetivamente). Todavia, a análise canónica de redundância demonstrou uma separação das amostras de acordo com o estado de infeção (P=0,030 e P=0,015, respetivamente), o que sugere uma correlação entre este e a composição da microbiota fecal felina.
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Ferrer, Clotas Marina. "Gut commensal microbiota and intestinal inflammation: modulatory role of rifaximin." Doctoral thesis, Universitat Autònoma de Barcelona, 2019. http://hdl.handle.net/10803/669498.
Full textAbstract:
Els trastorns funcionals gastrointestinals (síndrome de l'intestí irritable) i la malaltia inflamatòria intestinal presenten una inflamació crònica del tracte gastrointestinal. Encara que la seva patogènia no es coneix totalment, totes dues malalties resulten de la interacció de la microbiota amb factors ambientals que convergeixen en individus genèticament susceptibles, donant lloc a una activació anòmala del sistema immune. Els antibiòtics amb activitat immunomoduladora són una opció terapèutica interessant per la seva acció simultània davant la microbiota i la reacció immunitària. La rifaximina és un antibiòtic no absorbible aprovat pel tractament de la síndrome de l'intestí irritable amb diarrea i amb efectes beneficiosos en la malaltia inflamatòria intestinal. No obstant, es desconeix el seu mecanisme d'acció i la contribució dels seus efectes antimicrobians i immunomoduladors.
Aquest treball explora el mecanisme d'acció de la rifaximina en ratolins sans i durant la inflamació intestinal aguda. Es valoraren els efectes de la rifaximina en animals sans i en animals amb colitis aguda, utilitzant el model de colitis induïda per dextrà sulfat sòdic (DSS, 3% en aigua, 5 dies). Els ratolins es tractaren preventivament amb rifaximina o doxiciclina (control positiu). Es valoraren els signes clínics d'inflamació del còlon (macroscòpicament i histopatologia) en la necròpsia. La microbiota ceco-còlica, luminal i adherida a l'epiteli, es caracteritzarà mitjançant: hibridació in situ fluorescent (FISH), polimorfismes de longitud de fragments de restricció (T-RFLP) i seqüenciació del 16S ARNr. La resposta immune local i els mecanismes de interacció hoste-microbiota es valoraren determinant canvis en l'expressió gènica (RT-qPCR) de citocines pro- i antiinflamatòries, pèptids antimicrobians i receptors de tipus Toll (TLRs).
En animals sans, la rifaximina no va modificar els recomptes totals, la biodiversitat o la adherència a la paret del còlon dels bacteris ceco-còlics. Només es van observar canvis menors en l'expressió de TLRs o d'altres marcadors de tipus immune. Els animals que van rebre DSS van mostrar signes clínics indicatius del desenvolupament de colitis, amb regulació a l'alça en l'expressió de marcadors immunes, incloent el pèptid antimicrobià RegIIIɣ. La rifaximina no va afectar el curs clínic de la colitis ni l'expressió d'aquests marcadors. Per contra, la doxiciclina va atenuar les dues respostes. Independentment del tractament aplicat, només es van observar canvis menors en l'expressió de TLRs. L'expressió del receptor X de pregnà (PXR) va disminuir durant la inducció de la colitis, un canvi no modificat per la rifaximina, però que es va prevenir amb la doxiciclina. La colitis va induir una disbiosi caracteritzada per un augment de Verrucomicrobia i Deferribacteres amb un descens de Bacteroidetes, mantenint-se la diversitat de tipus alfa. Durant el tractament amb rifaximina, amb o sense colitis, es va mantenir la biodiversitat, amb una composició bacteriana molt similar a l'observada en animals sans. Els animals tractats amb doxiciclina van mostrar canvis extensos en la microbiota, amb similituds entre els grups inflamat i no inflamat. Concretament, la doxiciclina va reduir els grups Clostridiales patogènics, mentre que va augmentar els Clostridia grup XIVa, Lactobacillus i Ruminococcus, considerats grups beneficiosos.
Aquests resultats mostren que en animals sans la rifaximina presenta una activitat antimicrobiana i immunomoduladora limitada. En estat de colitis, la rifaximina no manifesta efectes immunomoduladors ni antimicrobians consistents amb una activitat antiinflamatòria. No obstant això, aquestes accions no es poden excloure en humans, explicant els efectes beneficiosos observats clínicament. Tenint en compte que en humans la rifaximina actuaria a través dels PXR, és possible que el model de colitis induïda per DSS en ratolí no sigui l'adequat per estudiar el seu mecanisme d'acció. (...)Los trastornos funcionales gastrointestinales (síndrome del intestino irritable) y la enfermedad inflamatoria intestinal presentan una inflamación crónica del tracto gastrointestinal. Aunque su patogenia no se conoce totalmente, ambas enfermedades resultan de la interacción de la microbiota con factores ambientales que convergen en individuos genéticamente susceptibles, dando lugar a una activación anómala del sistema inmune. Los antibióticos con actividad inmunomoduladora son una opción terapéutica interesante por su acción simultánea frente la microbiota y la reacción inmunitaria. La rifaximina es un antibiótico no absorbible aprobado para el tratamiento del síndrome del intestino irritable con diarrea y con efectos beneficiosos en la enfermedad inflamatoria intestinal. Sin embargo, se desconoce su mecanismo de acción y la contribución de sus efectos antimicrobianos e inmunomoduladores. Este trabajo explora el mecanismo de acción de la rifaximina en ratones sanos y durante la inflamación intestinal aguda. Se valoraron los efectos de la rifaximina en animales sanos y en animales con colitis aguda, utilizando el modelo de colitis inducida por dextrano sulfato sódico (DSS, 3% en agua, 5 días). Los ratones se trataron preventivamente con rifaximina o doxiciclina (control positivo). Se valoraron los signos clínicos de inflamación y el estado del colon (macroscópicamente e histopatología) en el momento de la necropsia. La microbiota ceco-cólica, luminal y adherida al epitelio, se caracterizó mediante: hibridación in situ fluorescente (FISH), polimorfismos de longitud de fragmentos de restricción (T-RFLP) y secuenciación del 16S ARNr. La respuesta inmune local y los mecanismos de interacción hospedador-microbiota se valoraron determinando cambios en la expresión génica (RT-qPCR) de citoquinas pro- y anti-inflamatorias, péptidos antimicrobianos y receptores de tipo Toll (TLRs). En animales sanos, la rifaximina no modificó los recuentos totales de bacterias ceco-cólicas, su biodiversidad o la adherencia bacteriana a la pared del colon. Sólo se observaron cambios menores en la expresión de TLRs o de otros marcadores de tipo inmune. Los animales que recibieron DSS mostraron signos clínicos indicativos del desarrollo de colitis, con regulación al alza en la expresión de marcadores inmunes, incluyendo al péptido antimicrobiano RegIIIɣ. La rifaximina no afectó el curso clínico de la colitis ni la expresión de dichos marcadores. Por el contrario, la doxiciclina atenuó ambas respuestas. Con independencia del tratamiento aplicado, sólo se observaron cambios menores en la expresión de TLRs. La expresión del receptor X de pregnano (PXR) disminuyó durante la inducción de la colitis, un cambio no modificado por la rifaximina, pero que se previno con la doxiciclina. La colitis indujo una disbiosis caracterizada por un aumento de Verrucomicrobia y Deferribacteres con un descenso de Bacteroidetes, manteniéndose la diversidad de tipo alfa. Durante el tratamiento con rifaximina, con o sin colitis, se mantuvo la biodiversidad, con una composición bacteriana muy similar a la observada en animales sanos. Los animales tratados con doxiciclina mostraron cambios extensos en la microbiota, con similitudes entre los grupos inflamado y no inflamado. Concretamente, la doxiciclina redujo los grupos Clostridiales patogénicos, mientras que aumentó los Clostridia grupo XIVa, Lactobacillus and Ruminococcus, considerados grupos beneficiosos. Estos resultados muestran que en animales sanos la rifaximina presenta una actividad antimicrobiana e inmunomoduladora limitada. En estado de colitis, la rifaximina no manifiesta efectos inmunomoduladores ni antimicrobianos consistentes con una actividad anti-inflamatoria. Sin embargo, estas acciones no pueden excluirse en humanos, explicando los efectos beneficiosos observados clínicamente. (...)
Inflammation of the gastrointestinal tract is a common component of functional gastrointestinal disorders (irritable bowel syndrome, IBS and inflammatory bowel disease, IBD). Evidences indicate that both arise because of a convergence of altered microbiota and external environmental factors in genetically susceptible individuals, leading to abnormal immune responses and the development of persistent inflammation, through a mechanism not fully understood. Given the important role of the microbiota and the immune system in their pathogenesis, immunomodulatory antibiotics are an interesting therapeutic approach, targeting simultaneously the microbiota and the exacerbated inflammatory response. Rifaximin is a non-absorbable antibiotic approved for the treatment of IBS with diarrhea and with beneficial effects in IBD. However, the mechanisms mediating these effects and the exact contribution of its antimicrobial and immunomodulatory activities are not fully understood. This work explores the mechanisms of action of rifaximin modulating gut microbiota and the local immune system in a healthy state and during acute intestinal inflammation using a dextran sulfate sodium (DSS)-induced colitis mouse model. First, healthy female mice were treated with either vehicle or rifaximin during 7 or 14 days. In a second study, colitis was induced with DSS (3% in water, 5 days). Mice were treated, in a preventive manner, with either rifaximin or doxycycline, serving as positive control. Daily clinical signs were recorded. At necropsy, colonic inflammation was assessed (macroscopic signs and histopathology). Luminal and wall-adhered ceco-colonic microbiota were characterized by fluorescent in situ hybridization (FISH), terminal restriction fragment length polymorphism (T-RFLP) and 16S rRNA gene sequencing. Local immune responses and host-bacterial interactions were determined assessing the expression (RT-qPCR) of pro- and anti-inflammatory cytokines, antimicrobial peptides and Toll-like receptors (TLRs). In healthy mice, rifaximin did not modify neither total ceco-colonic bacterial counts not microbial biodiversity. Moreover, rifaximin was associated to a minor upregulation of TLRs expression, without changes in the expression of immune-related markers. Animals receiving DSS showed clinical signs indicative of the development of colitis. Rifaximin did not affect the clinical course of colitis, while doxycycline attenuated clinical signs. Similarly, colitis-associated up-regulation of immune-related markers was not affected by rifaximin, while doxycycline completely prevented this response. As it relates to host-bacterial interaction markers, colitis selectively up-regulated the antimicrobial peptide RegIIIɣ, while it had minor effects on TLRs expression. Rifaximin did not affect colitis-associated RegIIIɣ up-regulation, while doxycycline completely normalized its expression. The pregnane X receptor (PXR) was down-regulated during colitis, a change not affected by rifaximin but prevented by doxycycline. DSS-induced colitis was associated to a dysbiotic state characterized by an increase in Verrucomicrobia and Deferribacteres and a simultaneous decrease in Bacteroidetes; with a maintenance of alpha diversity. During rifaximin treatment, with or without colitis, bacterial richness was maintained, with a bacterial composition closely related to that observed in healthy animals, vs. that observed during colitis. Doxycycline-treated animals showed extensive changes in their microbiota, with similarities between the inflamed and non-inflamed conditions. Particularly, doxycycline reduced pathogenic Clostridiales, while increased Clostridia cluster XIVa-related, Lactobacillus and Ruminococcus, considered beneficial groups. (...)
Books on the topic "Microbiota intestinale (Gut microbiota)"
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Olds, William. Health and the gut: The emerging role of intestinal microbiota in disease and therapeutics. Toronto: Apple Academic Press, 2015.
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Tannock, Gerald W., ed. Understanding the Gut Microbiota. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2017. http://dx.doi.org/10.1002/9781118801413.
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Pierre, Joseph F., ed. Metabolism of Nutrients by Gut Microbiota. Cambridge: Royal Society of Chemistry, 2022. http://dx.doi.org/10.1039/9781839160950.
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Chen, Peng, ed. Gut Microbiota and Pathogenesis of Organ Injury. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-2385-4.
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Marotta, Francesco, ed. Gut Microbiota in Aging and Chronic Diseases. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-14023-5.
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Kogut, Michael H., and Glenn Zhang, eds. Gut Microbiota, Immunity, and Health in Production Animals. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-90303-9.
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Kochhar, Sunil, and François-Pierre Martin, eds. Metabonomics and Gut Microbiota in Nutrition and Disease. London: Springer London, 2015. http://dx.doi.org/10.1007/978-1-4471-6539-2.
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Azcarate-Peril, M. Andrea, Roland R. Arnold, and José M. Bruno-Bárcena, eds. How Fermented Foods Feed a Healthy Gut Microbiota. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-28737-5.
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N.Y.) Nestlé Nutrition Workshop (79th 2013 New York. Nutrition, gut microbiota and immunity: Therapeutic targets for IBD. Edited by Lewis James D. editor, Ruemmele Frank M. editor, Wu Gary D. editor, and Nestlé Nutrition Institute. Basel, Switzerland: Karger, 2014.
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Lyte, Mark, and John F. Cryan, eds. Microbial Endocrinology: The Microbiota-Gut-Brain Axis in Health and Disease. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-0897-4.
Full textBook chapters on the topic "Microbiota intestinale (Gut microbiota)"
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Sartor, R. Balfour. "The Intestinal Microbiota in Inflammatory Bowel Diseases." In Nutrition, Gut Microbiota and Immunity: Therapeutic Targets for IBD, 29–39. Basel: S. KARGER AG, 2014. http://dx.doi.org/10.1159/000360674.
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Calo-Mata, Pilar, Jose Manuel Ageitos, Karola Böhme, and Jorge Barros-Velázquez. "Intestinal Microbiota: First Barrier Against Gut-Affecting Pathogens." In New Weapons to Control Bacterial Growth, 281–314. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-28368-5_12.
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Bortoluzzi, Cristiano, Fernanda Lima de Souza Castro, and Michael Kogut. "Butyrate and Intestinal Homeostasis: Effects on the Intestinal Microbiota and Epithelial Hypoxia." In Gut Microbiota, Immunity, and Health in Production Animals, 57–68. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-90303-9_4.
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Pool-Zobel, Beatrice L. "Diet and Biotransformation of Carcinogenic Compounds in the Gut by Enzymes of Microflora and of Intestinal Cells." In Colonic Microbiota, Nutrition and Health, 245–55. Dordrecht: Springer Netherlands, 1999. http://dx.doi.org/10.1007/978-94-017-1079-4_15.
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Rostagno, Marcos H. "Managing Intestinal Health in Farm Animals: A Critical View." In Gut Microbiota, Immunity, and Health in Production Animals, 1–12. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-90303-9_1.
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Rodrigues, Denise R. "Role of Early Life Intestinal Microbiota in Modulating Immunity in Broiler Chickens." In Gut Microbiota, Immunity, and Health in Production Animals, 225–42. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-90303-9_11.
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Perrigoue, Jacqueline, Anuk Das, and J. Rodrigo Mora. "Interplay of Nutrients and Microbial Metabolites in Intestinal Immune Homeostasis: Distinct and Common Mechanisms of Immune Regulation in the Small Bowel and Colon." In Nutrition, Gut Microbiota and Immunity: Therapeutic Targets for IBD, 57–71. Basel: S. KARGER AG, 2014. http://dx.doi.org/10.1159/000360685.
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Carey, Hannah V., Amanda C. Pike, Christopher R. Weber, Jerrold R. Turner, Annie Visser, Silvia C. Beijer-Liefers, Hjalmar R. Bouma, and Frans G. M. Kroese. "Impact of Hibernation on Gut Microbiota and Intestinal Barrier Function in Ground Squirrels." In Living in a Seasonal World, 281–91. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-28678-0_25.
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Chu, Fong-Fong. "Gut Microbiota." In Encyclopedia of Cancer, 1–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_7172-4.
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Chu, Fong-Fong. "Gut Microbiota." In Encyclopedia of Cancer, 1974–77. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-46875-3_7172.
Full textConference papers on the topic "Microbiota intestinale (Gut microbiota)"
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Andrade, Dariana Rodrigues, Letícia Mendes de Lima, Luis Henrique Goes Hamati Rosa, and Edvaldo Cardoso. "Brain-gut-microbiota axis in motor disorders." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.401.
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Introduction: There seems to be a strong relationship and influence on the brain-gut- microbiota axis in the control and prevention of several diseases, including degenerative diseases that are related to motor disorders. Objectives: To analyze the relationship between movement disorders and the intestinal microbiota. Methods: Integrative review performed at PUBMED, using the descriptors Movement disorder and intestinal microbiota, in the last five years and having as inclusion criteria complete texts in English. Results: The literature suggests that the intestinal microbiota regulates the activation of microglia through the production of bacteria metabolites. Gut dysbiosis is believed to generate metabolic disorders with decreased production of neuroprotective factors, increased pro-inflammatory cytokines, production of neurotoxins, and a misdirected immune response. Metabolites produced by an altered microbiota seem to enter the circulation and affect neurological function. Braak’s hypothesis postulates that aberrant accumulation of α-synuclein (αSyn), a central component of the pathophysiology of Parkinson’s disease (PD), begins in the intestine and propagates through the vagus nerve to the brain, given that αSyn inclusions previously arise in the enteric nervous system and glossopharyngeal and vagus nerves, and vagotomized individuals have reduced risk of PD. Conclusion: The identification of the microbiota or its altered metabolites may serve as biomarkers, or even drug targets for the treatment of diseases of the central nervous system. The microbiota can be modulated through antibiotic therapy, fecal microbiota transplantation, prebiotic supplementation, dietary interventions and many other potential methods.
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Lopes, Lorena Vieira, VINÍCIUS GRZECHOEZINSKI AUDINO, and GABRIEL STECHECHEN WIER. "EIXO INTESTINO-PULMÃO E O PAPEL DA MICROBIOTA INTESTINAL NA RESPOSTA À INFECÇÃO POR SARS-COV-2." In II Congresso Brasileiro de Imunologia On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/ii-conbrai/6286.
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Introdução: A microbiota intestinal está relacionada à modulação do sistema imunológico, influenciando no processo inflamatório e na resposta a infecções. No curso da COVID-19, uma resposta exacerbada, na conhecida “tempestade de citocinas”, gera hiperinflamação e é fator determinante da gravidade da doença. Objetivo: Analisar os efeitos da microbiota intestinal na regulação da resposta imunológica à infecção por SARS-CoV-2 e seus mecanismos. Metodologia: Realizou-se revisão da literatura, a partir de publicações indexadas na plataforma PubMed. Foram utilizados os descritores “COVID-19”, “microbiome”, “inflammation” e “gut-lung axis”. Após avaliação criteriosa, foram selecionados 5 artigos para a presente revisão. Resultados: Foram relatadas associações entre a microbiota intestinal e a mortalidade por infecções respiratórias, sugerindo a existência de um eixo de comunicação bilateral “intestino-pulmão”. O possível mecanismo dessa interação é a atuação da microbiota na imunidade inata antiviral do trato respiratório através da liberação de metabólitos e sinais imunomodulatórios que influenciam macrófagos alveolares, células epiteliais e células dendríticas. O microbioma modula a expressão de receptores Interferon tipo I e secreção de IFN-α e IFN-β, com efeito na restrição da replicação viral. A alteração da composição da microbiota intestinal (disbiose) possivelmente guarda correlação positiva com a gravidade da COVID-19: observou-se aumento de táxons patogênicos e diminuição daqueles conhecidos por sua ação protetora, conforme maiores as taxas de complicações. A composição bacteriana intestinal em pacientes com doença leve se mostrou mais próxima a controles, enquanto casos graves e fatais apresentaram importante diferença em relação às bactérias protetoras. Maiores níveis de citocinas inflamatórias foram correlacionados à alteração da microbiota intestinal em pacientes hospitalizados com COVID-19. A disbiose intestinal prévia, comum em pacientes com comorbidades e idade avançada, também está ligada à desregulação da resposta inflamatória ao SARS-CoV-2. Conclusão: Os mecanismos que ligam a microbiota intestinal à resposta à infecção por SARS-CoV-2 não são totalmente compreendidos. Porém, os resultados sugerem correlação entre a composição da microbiota intestinal, reação inflamatória e o curso da COVID-19, constituindo uma rota promissora à compreensão da patogênese e elaboração de estratégias que diminuam o impacto da doença. Dessa forma, mais estudos são necessários para que essa relação seja estabelecida.
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Oliveira, Nathália Brígida de, Anna Clara Silva Fonseca, Lailla Luísa Silva Gomes, Aline Balducci Ferreira Dos Santos, and Beatriz Martins Borelli. "ANÁLISE DA RELAÇÃO ENTRE A SÍNDROME DE LEAKY GUT, A MICROBIOTA INTESTINAL E DOENÇAS AUTOIMUNES: UMA REVISÃO BIBLIOGRÁFICA." In I Congresso Nacional de Microbiologia Clínica On-Line. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/1215.
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Introdução: Às células epiteliais do trato gastrointestinal participam da absorção de nutrientes e conferem proteção. Essa barreira é composta por junções estreitas, formando uma proteção física e conferindo a capacidade permeativa do intestino, e por uma camada de muco. Quando essas junções são agredidas por fatores imunológicos, citocinas ou patógenos, elas perdem a sua capacidade de selecionar o conteúdo intestinal e, assim, desenvolve a Síndrome do Intestino Permeável. Está disfunção se relaciona com inflamações sistêmicas e doenças autoimunes, o que ocorre, também pela alteração na composição da flora intestinal. Objetivos: Realizar revisão bibliográfica da literatura a respeito da correlação da Síndrome de Leaky gut e doenças autoimunes, bem como a importância da microbiota intestinal neste processo. Material e Métodos: A pesquisa foi realizada nas bases de dados SCIELO e PUBMED. Os descritores utilizados foram “autoimmune diseases”, “autoimmune disorders”, “gut microbiome”, “leaky gut” e “leaky gut syndrome”. Foram selecionados artigos acadêmicos originais, escritos na língua inglesa, que foram publicados entre 2014 e 2020. Tais artigos foram analisados de acordo com o ano de publicação, método de avaliação, objetivos e principais resultados. Resultados: A produção de moléculas pró-inflamatórias capazes de comprometer a integridade da barreira intestinal pode ser provocada por antígenos bacterianos intestinais. Esse quadro pode levar a síndrome de Leaky gut, o que explica a presença de bactérias intestinais no Sistema Imune, acarretando doenças autoimunes como: artrite reumatoide (AR), doença celíaca, Diabetes Mellitus tipo 1 (DM1). Na relação da AR e a permeabilidade intestinal, observou-se que indivíduos mais propensos a doenças tendem a ter um desequilíbrio da microbiota, gerando disbiose e contra regulação do sistema imune local e sistêmico à longo prazo e esse mesmo mecanismo ocorre com pacientes com AR. Conclusão: Considerando os dados obtidos, observou-se que há uma relação entre Leaky gut e a microbiota reduzida, como também a alteração funcional, tendo efeito na resposta imune principalmente em doenças autoimunes (AR, DM1 e doença celíaca). Percebe-se também que pela importância do tema há poucos estudos em humanos, o que demonstra a necessidade de mais pesquisas na área.
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Kozlovskaya, G. V., M. I. Zinevich, Y. E. Kozlovsky, T. I. Khomyakova, and A. D. Magomedova. "IMMUNOLOGICAL ASPECT OF ORAL ADMINISTRATION OF THE PROBIOTIC LACTOBACILLUS CASEI LB 148 UNDER COLD STRESS IN ANIMALS." In STATE AND DEVELOPMENT PROSPECTS OF AGRIBUSINESS Volume 2. DSTU-Print, 2020. http://dx.doi.org/10.23947/interagro.2020.349-351.
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Gut microbiome changes is considered as a basic causative factor of stress-associated diseases. Probiotics are usually used for the correction of disbiosis. The aim of the investigation was the study of the effects of oral probiotic Lactobacillus casei LB 148 use onto the gut microbiota as well as the number and total square of intestinal lymph nodules of rats Sprague Dawley at in health rats and under the cold stress
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Brenna, J. Thomas. "The gut microbiome and dietary fatty acids." In 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/rvcu7594.
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The dramatic increase in microbiome studies in the last 20 years, facilitated by high speed sequencing, has transformed our understanding of biology. Nutrition influences the easily measured distribution of organisms, and the more difficultly measured overall physiology of the microbiome. Fatty acid nutrition and its influence on the various gut microbiomes poses specific challenges for interpretation of experimental studies. Most microbiome science employs rodents as models. In rodents, fatty acids survive to the cecum and lower gut, while in healthy humans fatty acids are completely absorbed prior to the lower gut. Fatty acid nutrition influences the small intestine microbiome which has approximately 10-6 fewer microorganisms than the lower gut. Identification of microorganisms based on 18S ribosomal sequences usually does not identify organisms at the strain level (genus-species-strain) which determine the biology of specific organisms and how they interact within microbial ecology. Sustained consumption of specific oils causes shifts in microbiota organisms and evolution of organisms via natural selection, shown in the specific case of soy oil. Saturated branched chain fatty acids (BCFA) of carbon length from 11 to 26 carbons are absorbed in the upper gut and incorporated into enterocyte membranes. Sloughed enterocytes transport BCFA to the lower gut where they support increased levels of organisms that depend on BCFA for membrane function. Long chain BCFA appear at higher relative abundance in the fecal matter than in the diet as consumed. While some data are available on the interaction of specific fats and gut microbiome, most of the fundamental principles governing gut health and fat nutrition remain to be elucidated.
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Al Khatib, Heba, Muna Al Maslamani, Peter Coyle, Sameer Pathan, Asmaa Al Thani, and Hadi Mohamad Yassine. "Molecular Characterization of Influenza Virus in Intestines and its Effect on Intestinal Microbiota." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0165.
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Background: Influenza predominantly causes respiratory diseases; however, gastrointestinal symptoms are not uncommonly reported, particularly among high-risk groups. Influenza virus RNA has been also detected in stools of patients infected with pandemic and seasonal influenza, however, the role and the clinical significance of intestinal infection has not been clearly demonstrated. Methods: Here, we used NGS technology to investigate molecular characterization of viral RNA shedding in feces of adults with active influenza infection. Paired nasal and fecal samples were collected from 295 patients showing to emergency department at Hamad Medical Corporation with flu-like symptoms during January 2018 and April 2019. Results: Among these, 90 nasal samples were positive for influenza, of which, 26 fecal samples were positive for influenza in real-time PCR and only five showed virus growth in both monolayer and 3D cell culture. Full genome sequencing of isolated viruses revealed some unique mutations that we are currently in the process of studying their effect on virus kinetics. Then, we investigated the potential impact of respiratory influenza infection on intestinal microbiota diversity and composition. Microbiome analysis results suggest that changes in gut microbiota composition in influenza-infected patients are significantly associated with (1) influenza virus type, and (2) the presence of viral RNA in intestines of infected patients. We also identified bacterial taxa for which relative abundance was significantly higher in the patients with severe respiratory symptoms. Conclusion: Altogether, our findings suggest that influenza viruses can affect intestinal environment either by direct intestinal infection or indirectly by modulating intestinal microbiota.
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Orlenkovich, Lilija. "CORRELATIONS ANALYSIS OF IMMUNE SYSTEM AND GUT MICROBIOTA INDICES OF RATS IN THE CHRONIC EXPOSITION TO BIOINSECTICIDE ENTOMOPHTHORIN." In XIV International Scientific Conference "System Analysis in Medicine". Far Eastern Scientific Center of Physiology and Pathology of Respiration, 2020. http://dx.doi.org/10.12737/conferencearticle_5fd728a1ea3837.21988844.
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The analysis of the variation in the number, intensity and direction of correlations between the immune system and the gut microbiota of rats revealed that the T-, B-system and humoral immunity changes as well as cellular and humoral factors of an organism nonspecific defense are accompanied by changes of the Intestinal microbiota of intact and experimental rats
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Thomas, John P., Aimee Parker, Devina Divekar, Carmen Pin, and Alastair Watson. "PTU-066 The gut microbiota influences intestinal epithelial proliferative potential." In British Society of Gastroenterology, Annual General Meeting, 4–7 June 2018, Abstracts. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2018. http://dx.doi.org/10.1136/gutjnl-2018-bsgabstracts.407.
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Nogueira, Fábio Dias, Ana Klara Rodrigues Alves, Barbara Beatriz Lira da Silva, Ana Kamila Rodrigues Alves, Marlilia Moura Coelho Sousa, Ana Karla Rodrigues Alves, Wanderson da Silva Nery, Breno Carvalho de Almeida, Flávia Dias Nogueira, and Leiz Maria Costa Véras. "The autistic spectrum disorder and its relation to intestinal dysbiosis." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.283.
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Introduction: Autistic Spectrum Disorder (ASD) is characterized by a neurodevelopmental disorder, in which the child has persistent deficits in verbal and / or non-verbal communication, social interaction and behavior. One of the factors related to the cause of ASD are nutritional aspects, such as intestinal dysbiosis. Objective: To analyze the relationship between imbalance in the intestinal microbiota and the pathophysiological characteristics of ASD. Methodology: This is a systematic review, carried out in the Pubmed, SciELO databases, in order to answer the question: what is the relationship between intestinal microbiota imbalance and ASD? 139 articles were found, of which 12 were selected, through the simultaneous crossing between the descriptors “Autistic Disorder”, “Dysbiosis”. Articles written in Portuguese and English published from 2016 to 2021 were inserted. Results/Discussion: Most children with ASD exhibit gastrointestinal symptoms, such as constipation and diarrhea, and greater intestinal permeability, with major differences in the composition of microorganisms in the gastrointestinal tract (GIT). Patients with ASD have a lower microbiota diversity in the GIT. However, it is not possible to identify the origin of this change, since children with ASD often have changes in diet and eating behavior, which could alter the microbiota. Conclusion: It is still complex to understand what are the main causes of ASD. The gut-brain axis is an important associated factor both in the etiology and in the clinical manifestations of ASD. The use of diets, together with the modulation of the microbiota, by the use of probiotics and specific antibiotics, are possibilities for promising therapy.
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Maia, Lucas Henrique, Thaís Galdino Diniz, Vitor Carvalho Caetano, Marina Gomes Diniz, Pedro Lucas Bessa dos Reis, Gabriela Vieira Marques da Costa Leão, Vitor Moreira Nunes, and Helton José dos Reis. "Antibiotic therapy as a risk factor in Parkinson’s disease." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.521.
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Background: Antibiotics exposure is related to gastrointestinal tract dysbiosis and appearance of systemic repercussions. Due to the correlation between Enteric Nervous System (ENS) and Central Nervous System (CNS), abnormalities in the gut microbiota have been associated with neurological disorders including Parkinson’s Disease (PD). Objectives: Search evidence in the scientific literature relating antibiotic therapy and Parkinson’s disease. Methods: A systematic review has been done using the descriptors “Parkinson’s disease”, “antibiotics” and “gut microbiota” in PubMed’s database. The research was conducted in april 2021, without temporal limitations, in english and portuguese. Results: Studies suggest that PD begins with intestinal inflammation and abnormal alpha-synuclein deposition in the ENS that follows, through nerves, to the CNS. Results show that leaky gut and dysbiosis preceded 5-10 years PD’s initial symptoms, while the intense exposure to antibiotics preceded 10-15 years the diagnostic. On average, PD patients received larger amounts of antibiotics than controls (p=0.021). Dysbiosis post-antibiotics presented reduced diversity of Bacteroidetes, Firmicutes and Prevotellaceae and growthing of Enterobacteriaceae, resulting in higher risk of gastrointestinal infections, higher rates of pro-inflammatory cytokines, increased permeability of gastrointestinal and brain-blood barriers and hyperexpression of the alpha-synuclein protein in the colon. Conclusion: Poorly controlled antibiotic therapy and its subsequent damage to gut microbiota anticipates PD’s early symptoms.
Reports on the topic "Microbiota intestinale (Gut microbiota)"
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yu, luyou, jinping yang, xi meng, and yanhua lin. Effectiveness of the gut microbiota-bile acid pathway (BAS) in the treatment of Type 2 diabetes: A protocol for systematic review and meta analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, July 2022. http://dx.doi.org/10.37766/inplasy2022.7.0117.
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Review question / Objective: To systematically evaluate the efficacy of the intestinal microbiome - bile acid pathway (BAS) in the treatment of T2DM. Condition being studied: Bile acids (BAs), an important component of bile, are also metabolites derived from cholesterol and promote intestinal absorption and transportation of dietary lipids . Studies have shown that bile acid receptor agonists can promote glP-1 secretion and improve glucose metabolism in preclinical mouse models of obesity and insulin resistance , which may become a new therapeutic target for Type 2 diabetes. However, no systematic review and meta-analysis has been found on the treatment of type 2 diabetes by intestinal microbiome - bile acid pathway. Therefore, we conducted a systematic review and meta-analysis to evaluate the safety and effectiveness of intestinal microbiome-bile acid pathway in the treatment of type 2 diabetes.
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Schokker, Dirkjan, Petra Roubos, Evelien Alderliesten, Arie Kies, Els Willems, and Mari Smits. Integration of multiple gut microbiota datasets of pigs and broilers. Wageningen: Wageningen Livestock Research, 2017. http://dx.doi.org/10.18174/426339.
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Gong, Boshen, Fanrui Meng, and Yang Yang. Association Between Gut Microbiota and Autoimmune Thyroid Disease: A Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2021. http://dx.doi.org/10.37766/inplasy2021.4.0135.
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Yang, zeqi, qiuhong Guo, yangyang Han, fan Gao, jiaye Tian, and ran Bai. Effects of traditional chinese medicine intervention on the gut microbiota in patients with chronic heart failure. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2022. http://dx.doi.org/10.37766/inplasy2022.6.0006.
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Huang, Li, Xin Luo, and Ming Chen. Effect of Traditional Chinese Medicine on Gut Microbiota with Chronic Kidney Disease: A Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, October 2021. http://dx.doi.org/10.37766/inplasy2021.10.0118.
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Huang, Langlang, Jianan Wang, Ri Xu, Yanwei Liu, and Zhongyong Liu. Regulatory effect of traditional Chinese medicine on gut microbiota in patients with atherosclerosis：A protocol for systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2020. http://dx.doi.org/10.37766/inplasy2020.11.0056.
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Jiang, Qiong, Zhong Cao, Yu Zhang, Ju Qiu, Hui Chen, and Jia Li. Effects of acupuncture and moxibustion on the gut microbiota of Irritable Bowel Syndrome (IBS): a protocol for the systematic review and meta-analysis of randomized controlled trials in animal models. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2022. http://dx.doi.org/10.37766/inplasy2022.5.0118.
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Grueso-Navarro, Elena, Leticia Rodríguez-Alcolado, Ángel Arias, Emilio J. Laserna-Mendieta, and Alfredo J. Lucendo. Influence of HLA-DQA1*05 allele in the response to anti-TNFα drugs in inflammatory bowel diseases. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, February 2023. http://dx.doi.org/10.37766/inplasy2023.2.0076.
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Review question / Objective: Do patients with inflammatory bowel disease and treated with any anti-TNFα drug who had the HLA-DQA1*05 allele (in heterozygosis or homozygosis) have lower response or persistence to those drugs than patients without HLA-DQA1*05 allele? Condition being studied: Inflammatory bowel diseases (IBD), which includes Crohn’s disease (CD) and ulcerative colitis (UC), is a chronic inflammatory condition that may affect any part of the digestive tract (CD) or be limited to the colon (UC). While the specific aetiology of IBD remains unknown, it is believed to involve a complex impairment in the immunity of the gut mucosa due to a combination of several genetic and environmental factors, being the microbiota one of the latest that more attraction has received in recent years. Symptoms of IBD (such as abdominal pain, diarrhoea, fever, tiredness or rectal bleeding) may be either constant or alternate between periods of limited disease activity and flares with remarkable presence of symptoms. As IBD is associated with significant morbidity and disability, pharmacological treatment is required in most cases, especially in CD, aimed at reducing the inflammatory response and attenuating the activity of the immune system. In the moderate and severe forms of the disease, therapy is usually based on immunosuppressant and/or biological drugs. Among the latest, anti-TNFα drugs (infliximab or adalimumab) are normally chosen as the initial biological therapy.