81 research outputs found

    Gut microbiota related to Giardia duodenalis, Entamoeba spp. and Blastocystis hominis infections in humans from CĂŽte d'Ivoire.

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    INTRODUCTION: Literature data provide little information about protozoa infections and gut microbiota compositional shifts in humans. This preliminary study aimed to describe the fecal bacterial community composition of people from Cîte d'Ivoire harboring Giardia duodenalis, Entamoeba spp., and Blastocystis hominis, in trying to discover possible alterations in their fecal microbiota structure related to the presence of such parasites. METHODOLOGY: Twenty fecal samples were collected from people inhabiting three different localities of Cîte d'Ivoire for copromicroscopic analysis and molecular identification of G. duodenalis, Entamoeba spp., and B. hominis. Temporal temperature gradient gel electrophoresis (TTGE) was used to obtain a fingerprint of the overall bacterial community; quantitative polymerase chain reaction (qPCR) was used to define the relative abundances of selected bacterial species/group, and multivariate statistical analyses were employed to correlate all data. RESULTS: Cluster analysis revealed a significant separation of TTGE profiles into four clusters (p < 0.0001), with a marked difference for G. duodenalis-positive samples in relation to the others (p = 5.4×10-6). Interestingly, qPCR data showed how G. duodenalis-positive samples were related to a dysbiotic condition that favors potentially harmful species (such as Escherichia coli), while Entamoeba spp./B. hominis-positive subjects were linked to a eubiotic condition, as shown by a significantly higher Faecalibacterium prausnitzii-Escherichia coli ratio. CONCLUSIONS: This preliminary investigation demonstrates a differential fecal microbiota structure in subjects infected with G. duodenalis or Entamoeba spp./B. hominis, paving the way for using further next-generation DNA technologies to better understand host-parasite-bacteria interactions, aimed at identifying potential indicators of microbiota changes

    Eubiosis and dysbiosis: the two sides of the microbiota

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    The microbial ecosystem of the gastrointestinal tract is characterized by a great number of microbial species living in balance by adopting mutualistic strategies. The eubiosis/dysbiosis condition of the gut microbiota strongly influences our healthy and disease status. This review briefly describes microbiota composition and functions, to then focus on eubiosis and dysbiosis status: the two sides of the microbiot

    A distinctive 'microbial signature' in celiac pediatric patients

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    <p>Abstract</p> <p>Background</p> <p>Celiac Disease (CD) is an autoimmune disorder of the small intestine in which dietary gluten ingestion leads to a chronic enteropathy. Recently, scientific evidence suggested a potential role of gut microbiota in CD. To have a snapshot of dominant duodenal microbiota we analyzed the mucosa-associated microbiota of 20 children with CD, before and after a gluten-free diet (GFD) regimen, and of 10 controls. Total DNA was extracted from duodenal biopsies and amplification products of 16S ribosomal DNA were compared by temporal temperature gradient gel electrophoresis (TTGE). TTGE profiles were analyzed by statistical multivariate analysis.</p> <p>Results</p> <p>The average number of bands in TTGE profiles was significantly higher (<it>P </it>< 0.0001) in active (n.b. 16.7 ± 0.7) and inactive states (n.b. 13.2 ± 0.8) than in controls (n.b. 3.7 ± 1.3). Mean interindividual similarity index was 54.9% ± 14.9% for active disease, 55.6% ± 15.7% for remission state and 21.8% ± 30.16% for controls. Similarity index between celiac children before and after GFD treatment was 63.9% ± 15.8%. Differences in microbiota biodiversity were among active and remission state (<it>P </it>= 0.000224) and amid active CD and controls (<it>P </it>< 0.001). <it>Bacteroides vulgatus </it>and <it>Escherichia coli </it>were detected more often in CD patients than in controls (<it>P </it>< 0.0001).</p> <p>Conclusions</p> <p>Overall, the results highlighted a peculiar microbial TTGE profile and a significant higher biodiversity in CD pediatric patients' duodenal mucosa. The possible pathophysiological role of these microbial differences needs further characterization.</p

    Nox2-deficient Tregs improve heart transplant outcomes via their increased graft recruitment and enhanced potency.

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    Nox2 is a ROS-generating enzyme, deficiency of which increases suppression by Tregs in vitro and in an in vivo model of cardiac remodelling. Since Tregs have emerged as a candidate therapy in autoimmunity and transplantation, we hypothesised that Nox2 deficiency in Tregs in recipient mice may improve outcomes in a heart transplant model. A novel B6129 mouse model with Treg-targeted Nox2 deletion (Nox2fl/flFoxP3Cre+) was generated and transplanted with hearts from CB6F1 donors. As compared to littermate controls, Nox2fl/flFoxP3Cre+ mice had lower plasma levels of alloantibodies and troponin-I, reduced levels of IFN-Îł in heart allograft homogenates and diminished cardiomyocyte necrosis and allograft fibrosis. Single cell analyses of allografts revealed higher absolute numbers of Tregs and lower CD8+ T cell infiltration in Nox2-deficient recipients compared to Nox2-replete mice. Mechanistically, in addition to a greater suppression of CD8+CD25- T effector cell proliferation and IFN-Îł production, Nox2-deficient Tregs expressed higher levels of CCR4 and CCR8, driving cell migration to allografts; this was associated with increased expression of miR214-3p. These data indicate that Nox2 deletion in Tregs enhances their suppressive ability and migration to heart allografts. Therefore, Nox2 inhibition in Tregs may be a useful approach to improve their therapeutic efficacy

    Intestinal microbiota influences clinical outcome and side effects of early breast cancer treatment.

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    The prognosis of early breast cancer (BC) relies on cell autonomous and immune parameters. The impact of the intestinal microbiome on clinical outcome has not yet been evaluated. Shotgun metagenomics was used to determine the composition of the fecal microbiota in 121 specimens from 76 early BC patients, 45 of whom were paired before and after chemotherapy. These patients were enrolled in the CANTO prospective study designed to record the side effects associated with the clinical management of BC. We analyzed associations between baseline or post-chemotherapy fecal microbiota and plasma metabolomics with BC prognosis, as well as with therapy-induced side effects. We examined the clinical relevance of these findings in immunocompetent mice colonized with BC patient microbiota that were subsequently challenged with histo-compatible mouse BC and chemotherapy. We conclude that specific gut commensals that are overabundant in BC patients compared with healthy individuals negatively impact BC prognosis, are modulated by chemotherapy, and may influence weight gain and neurological side effects of BC therapies. These findings obtained in adjuvant and neoadjuvant settings warrant prospective validation

    What is new about diet in hepatic encephalopathy

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    There is a relationship between hepatic encephalopathy (HE) protein malnutrition and muscle wasting. Muscle may play an alternative role in ammonia detoxification. Molecular mechanisms responsible for muscle depletion are under investigation. Specific nutrients may interact to reverse the molecular pathways involved in muscle wasting at an early stage. Training exercises have also been proposed to improve skeletal muscle mass. However, these data refer to small groups of patients. The amelioration of muscle mass may potentially help to prevent HE. The pathogenesis of HE is associated with modifications of the gut microbiota and diet is emerging to play a relevant role in the modulation of the gut milieu. Vegetarian and fibre-rich diets have been shown to induce beneficial changes on gut microbiota in healthy people, with reduction of Bacteroides spp., Enterobacteriaceae, and Clostridium cluster XIVa bacteria. By way of contrast, it has been suggested that a high-fat or protein diet may increase Firmicutes and reduce Bacteroidetes phylum. Milk-lysozyme and milk-oligosaccharides have also been proposed to induce a "healthy" microbiota. At present, no studies have been published describing the modification of the gut microbiota in cirrhotic patients with HE as a response to specific diets. New research is needed to evaluate the potentiality of foods in the modulation of gut microbiota in liver disease and HE

    GUT MICROBIOTA AND THE IMMUNE SYSTEM: AN INTIMATE PARTNERSHIP IN HEALTH AND DISEASE

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    In recent years there have been increased rates of autoimmune diseases, possibly associated to altered intestinal microflora. In this brief review article, after a description of the structure and function of the gut microbiota organ and its cross-talk with the human host, we give a report on findings indicating how the host immune system responds to bacterial colonization of the gastrointestinal tract. The disturbances in the bacterial microbiota will result in the deregulation of adaptive immune cells, which may underlie autoimmune disorders. The mammalian immune system, which seems to be designed to control microorganisms, could be instead influenced by microorganisms, as suggested in recent literature. Alterations in both the structure and function of intestinal microbiota could be one of the 'common causative triggers' of autoimmune and/or autoinflammatory disorders

    The Microbiota in Inflammatory Bowel Disease in Different Age Groups

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    Background: Many efforts were made in the past decades to assess the role of gut microbiota in inflammatory bowel diseases (IBD), leading to the hypothesis that an altered microbial composition, other than the presence of a specific pathogen, could be involved in the pathogenesis of the disease. On the other hand, existing differences in gut microbial community between distinct classes of age make sense of an increasing research in microbial shifts in IBD. Methods: Cultural, molecular, metabolomic and metagenomic approaches are trying to define the human gut microbiota in different age groups. Results and Conclusion: An increase in anaerobic bacteria (Bacteroides vulgatus, Streptococcus faecalis) was observed in adult IBD, whereas an increase in aerobic and facultative-anaerobic (Escherichia coli) was found in pediatric IBD. Overall higher bacterial cell counts were observed in IBD, jointly with a general loss of biodiversity and a preponderance of Bacteroidetes and a parallel decrease of Firmicutes phylum : a predominance of potential harmful members of Proteobacteria (E. coli) and low abundance of beneficial species (Faecalibacterium prausnitzii) was also reported in pediatric and adult age groups, respectively. Microbial community of elderly subjects contains a wider range of different species than those of children and adults, both in healthy and IBD status. Copyright (C) 2009 S. Karger AG, Base

    Gut microbiota and pediatric disease

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    Background: Researchers have made every effort to assess the role of gut microbiota in pediatric diseases like inflammatory bowel disease (IBD), celiac disease, asthma, allergy, and autism. The leading hypothesis is that an altered microbial composition is present (other than the presence of a specific pathogen) and that it could be involved in the pathogenesis or progression of such disorders. Methods: Cultural, molecular, metabolomic, and metagenomic approaches are trying to define the pediatric gut microbiota imbalances in different diseases. Results and Conclusion: In pediatric IBD, a marked increase in aerobes and facultative anaerobes was found, along with an increase in Enterobacteriaceae members (Escherichia coli). In both pediatric IBD and celiac disease (Th1-mediated disorders), higher bacterial cell counts were observed, jointly with a general gain of biodiversity. A preponderance of Bacteroidetes and a parallel decrease of Firmicutes was also reported in IBD, celiac disease and autism. Contrarily, dietary changes due to Western lifestyles increase Firmicutes populations and lower short-chain fatty acids production, possibly exposing 'developed' children to the infectious challenge (Escherichia and Shigella spp.). Lactobacillus and Bifidobacterium species could be protective agents for atopic diseases, while Clostridia, Enterobacteriaceae, and staphylococci can be associated with an increased risk of such Th2-mediated disorders. In the brain-gut axis view, gut microbiota could also play a role in autism. Copyright (C) 2011 S. Karger AG, Base
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