Добірка наукової літератури з теми "Flore intestinale – Greffe – Recherche"
Оформте джерело за APA, MLA, Chicago, Harvard та іншими стилями
Зміст
Ознайомтеся зі списками актуальних статей, книг, дисертацій, тез та інших наукових джерел на тему "Flore intestinale – Greffe – Recherche".
Біля кожної праці в переліку літератури доступна кнопка «Додати до бібліографії». Скористайтеся нею – і ми автоматично оформимо бібліографічне посилання на обрану працю в потрібному вам стилі цитування: APA, MLA, «Гарвард», «Чикаго», «Ванкувер» тощо.
Також ви можете завантажити повний текст наукової публікації у форматі «.pdf» та прочитати онлайн анотацію до роботи, якщо відповідні параметри наявні в метаданих.
Дисертації з теми "Flore intestinale – Greffe – Recherche"
Le, Roy Tiphaine. "Implication du microbiote intestinal dans l’insulino-résistance et les pathologies hépatiques associées à l’obésité, étude sur modèle murin." Electronic Thesis or Diss., Paris, AgroParisTech, 2012. http://www.theses.fr/2012AGPT0016.
Повний текст джерелаObesity predisposes people to several severe pathologies, including type 2 diabetes and NAFLD (Non Alcoholic Fatty Liver Disease). Such pathologies are characterized by insulin resistance and systemic low grade inflammation. Recently, it has been established that such pathologies are associated to a gut microbiota dysbiosis. Moreover, recent studies in mice and human indicate that modulation of gut microbiota composition has beneficial effects on people suffering type 2 diabetes and/or NAFLD. Otherwise, it has been showed that germ-free mice remain lean, normo-glycemic and sensitive to insulin when fed a high-fat diet.The aim of this study was i) to decipher to what extent the pathogenesis of insulin resistance and NAFLD depends on the presence or absence of gut microbiota, ii) to determine if the predisposition to metabolic disorders in an obesity context can be transferred via gut microbiota transplantation.We first compared the response of germ-free and conventional mice to high fat diet. Indeed, germ-free mice appeared to be resistant to high-fat diet-induced obesity and insulin resistance. However, germ-freeness only partially protects against diet-induced steatosis, that is to say accumulation of triglycerides in hepatocytes. In conventional mice, high-fat diet induced an increase of the hepatic expression of genes involved in lipogenesis. The inverse phenomenon was observed in germ-free mice. In order to study the liver inflammation, we isolated and cultivated liver macrophages from the two groups of mice. As in conventional mice, high-fat diet induced an increased secretion of pro-inflammatory cytokines by germ-free mice liver macrophages. However, germ-free mice macrophages remained sensitive to LPS stimulation, which was not observed in the conventional mice group. This results demonstrates that being devoid of gut microbiota deeply alters the immunological and metabolic responses to high-fat diet. Therefore, differences in gut microbiota composition could explain the differences of susceptibility in diet-induced insulin-resistance and NAFLD.Then, we colonised two groups of germ-free mice with the gut microbiota of two conventional mice the responses of which to high-fat diet were discrepant. The two donors mice presented different levels of fasting glycemia and HOMA-IR index despite a similar body weight. Both groups of colonised mice developped comparable obesity but different degrees of fasting glycemia and insulin resistance. Levels of steatosis and hepatic expression of genes involved in lipogenesis were as well different in the two groups of colonised mice. Hence the results clearly show that the gut microbiota is the cause of the predisposition to diet-induced insulin resistance and hepatic steatosis. Gut microbiota analysis revealed a higher proportion of lactic acid bacteria, Atopobium, Bacteroides and Akkermansia muciniphila in receiver mice resistant to diet-induced insulin resistance and steatosis, which allow us to hypothesize a protective effect of these bacteria in diet-induced metabolic disorders
Chamignon, Célia. "Identification de souches bactériennes à potentiel probiotique dans la diminution des hyperperméabilités intestinales et détermination de leur(s) mécanisme(s) d’action." Thesis, université Paris-Saclay, 2020. http://www.theses.fr/2020UPASA011.
Повний текст джерелаThe gastro-intestinal tract represents the largest interface between the human body and its environment. It is a multilayer system composed of mucus and epithelial cells that establish and regulate barriers, while directly connecting to the immune system. This interface allows fluxes of water and nutriments and prevents from the entry of antigens and pathogens. Thus, it is the first line of defense. The regulation of the permeability occurs through the paracellular pathway, which is supported by the epithelial complex of junctional proteins. The gut microbiota also plays a key role in the regulation of the immune and metabolic systems and also, in the protection against pathogens. The continuous cross-talks between the intestinal barrier and the microbiota are essential to maintain the intestinal integrity and therefore the global homeostasis in healthy conditions. Nowadays, most of the chronic syndromes and diseases, such as irritable bowel syndrome (IBS) but also metabolic or behavioral disorders, are associated with an increase of the gut permeability also called “leaky gut syndrome”. Indeed, the consequence of the hyperpermeability is a flow increase of water and nutriments across the intestinal barrier but also of pathogens or toxins, among others, promoting an immune response and inflammation. Many studies also associated changes in the gut microbiota composition, dysbiosis, with chronic diseases. The beneficial effects of probiotic strains are increasingly demonstrated from in vitro experimentations to clinical trials and these studies demonstrated that they can be used in both the prevention and treatment of these disorders. We aimed to better decipher the interactions between the intestinal epithelial components and the probiotic bacteria in the pathophysiological context of intestinal chronic disorders. To do that, we first designed an in vitro screening of over fifty strains, from different genus, based on trans-epithelial electrical resistance (TEER) of two types of human intestinal epithelial cell lines, Caco-2 and T84. With these models, six Lactobacillus strains were selected and we better characterized their probiotic properties (adhesion ability, biofilm stability, neurotransmitter production and enzyme activity). We further evaluated the effect of four of them in in vivo models of chronic low-grade inflammation and neonatal maternal separation using C57BL/6J mice. Finally, we determined the implication of the bacterial strains in the modulation of the gut permeability, through the study of the complex of cellular junctional proteins
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.
Повний текст джерелаAmong 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
Daillere, Romain. "Impact du microbiote intestinal sur l’efficacité anti-tumorale de la chimiothérapie par cyclophosphamide." Thesis, Université Paris-Saclay (ComUE), 2015. http://www.theses.fr/2015SACLS073.
Повний текст джерелаMore than 50 years after its approval by the Food and Drug Administration, cyclophosphamide (CTX) remains a drug with miscellaneous properties currently used in anti-cancer chemotherapy. This cytotoxic agent has immuno-modulatory properties and stimulate anti-tumoral immune responses. At metronomic doses, CTX induces the polarisation of splenocytes toward a Th1 and Th17 profile, characterized by the secretion of IFN et IL-17, both mandatory for the tumoricidal activity of this drug. CTX, as cytotoxic agent, targets proliferating cells, either normal or tumoral. Indeed, CTX is responsible for disrupting the gut barrier integrity as well as intestinal homeostasis. We have shown that people treated with CTX have a weaker intestinal barrier which breaks the tolerance toward the intestinal microbiota and leads to its immunization against some bacterial strains. This immunization is composed of CD4+ effector lymphocytes called « pathogenic Th17 » producing IFN and IL-17, which helps tumor-infiltrating lymphocytes to control the tumor growth in mice. Broad spectrum antibiotics as well as vancomycin (which mainly kills Gram positive bacteria) and colistin (which mainly eliminates Gram negative bacteria) all compromised the full-blown anticancer activity of CTX in vivo. Moreover, we have identified two bacteria, Enterococcus hirae and Barnesiella intestinihominis, able to rescue the efficacy of CTX abolished with antibiotics. E. hirae, a Gram+ bacterium, elicits Th1 immune responses and pathogenic Th17 cells capable of enhancing tumor-specific CD4+ and CD8+ T cell responses against candidate tumor antigens associated with tumor control. B. intestinihominis, a Gram- bacterium, was able to rescue the long term cognate responses lost with broad spectrum antibiotics or colistin treatment. Our data underscore the role of the gut microbiota in the efficacy of chemotherapy by CTX
Burz, Sebastian D. "Implication du microbiote intestinal humain dans l‘évolution des hépatopathies métaboliques non liées à l’alcoolisme (NAFLD)." Thesis, université Paris-Saclay, 2020. http://www.theses.fr/2020UPASA004.
Повний текст джерелаNon-alcoholic fatty liver diseases (NAFLD) include a spectrum of liver diseases ranging from fatty liver (NAFL), going through fibrosis (NASH), then cirrhosis in the absence of alcohol consumption, viral infection or other identified causes, and sometimes the development of hepatocellular carcinoma (HCC). Due to its high prevalence, up to a quarter of the general European population and its harmful consequences on the health of those who suffer from it, NAFLD represent a major public health issue.This liver disease has been associated with changes in gut microbiota and metabolic pathways in which this microbiota is involved. In mice, gut microbiota contributes to the worsening or protection of this disease.The goal of the thesis is to determine whether in humans the gut microbiota contributes also to this individual susceptibility observed in NAFLD mice.A complete standardized procedure for preparing, storing and managing human fecal transplants is developed and implemented (Burz et al., 2019).Specific pathogens free mice (SPF), pretreated with a cocktail of antibiotics, were colonized with microbiota derived from an healthy individual or patients at different stages of NAFLD. Then these mice were challenged with a high fructose, high fat diet in order to explore the effect of installed human microbiota on the onset and progression of induced NAFLD.This project made it possible to demonstrate, through the transfer of the human fecal microbiota, with constant food energy intake, the transfer of overweight. The human NAFL fecal microbiota worsens liver steatosis in mice, but mitigates liver and caecal inflammation.This thesis sheds additional light on the impact of gut microbiota in the establishment of the natural pathophysiology of NAFLD, especially during the early phase of the disease. The project also generated additional knowledge that could be developed in future projects in order to establish therapeutic strategies targeting gut microbiota. This set constitutes an important achievement in a very competitive research field, which generates major interest for food and pharmaceutical industries, and thus supports the international development of the different partners of the project
Mir, Hayatte-Dounia. "Influence de l'indole produit par le microbiote intestinal sur les comportements émotionnels chez la souris." Thesis, Université Paris-Saclay (ComUE), 2018. http://www.theses.fr/2018SACLA041/document.
Повний текст джерелаDepression is the most spread neuropsychiatric disorder worldwide. It is a socio-economical burden and efficacy of the treatments is very limited. Mechanisms underlying this disorder are mainly unknown. However, a growing number of data has highlighted the potential role of gut microbiota dysbioses in the pathophysiology of depression. Particularly, an unbalance in the diversity and abundance of metabolites produced by the gut microbiota might be implicated. Indole is a tryptophan derivative produced by the gut microbiota. It is known to influence (i) the bacterial physiology and quorum sensing within the gut microbial ecosystem, (ii) the intestinal cells functioning, and (iii) some of its derivatives are known to affect the brain. The aim of this work is to investigate how an overproduction of indole by the gut microbiota can modulate the brain and behaviour in the context of depression and its main co-morbidity, anxiety. This thesis work contains 3 sections.In the first one, we investigated whether an intestinal microbiota dysbiosis leading to an overproduction of indole could confer vulnerability toward anxiety and depression. We also looked for potentially associated biochemical and molecular changes. A behavioural study in gnotobiotic mice overproducing or non producing indole showed the overproduction of indole exacerbated the anxiety-like and depressive-like behaviours induced by a chronic mild stress. Gene expression analysis in the adrenal glands showed chronically stressed mice overproducing indole up-regulated the expression of one gene implicated in adrenaline synthesis. Brain neurotransmitters quantification and gene expression in the brain and intestinal mucosa were also carried out. The second part of the thesis work focused on the brain neurocircuitry of indole. Conventional mice were force-fed with indole and the c-Fos protein was labelled by immunohistochemistry in all brain areas from brainstem to prefrontal cortex. In the third and last part, we modulated dietary tryptophan availability in the gastro-intestinal tract of mice, to study how this modulation could affect the composition and the indole production ability of the gut microbiota. The mice fecal microbiota composition was determined by 16S rRNA sequencing, and fecal tryptophan and indole concentrations were measured by HPLC.In summary, this work improves the understanding of the role of indole in the behavioural and neuro-endocrine responses to stress. This study also initiated the deciphering of brain circuits activated by indole. Finally, it brings some evidence about how modulating food digestibility can impact the gut microbiota composition and its indole production capacity