Relevant bibliographies by topics / MICROBIAL DYSBIOSIS

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  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers

Academic literature on the topic 'MICROBIAL DYSBIOSIS'

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Published: 9 March 2023

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Journal articles on the topic "MICROBIAL DYSBIOSIS"

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Nath, SameeraG, and Ranjith Raveendran. "Microbial dysbiosis in periodontitis." Journal of Indian Society of Periodontology 17, no. 4 (2013): 543. http://dx.doi.org/10.4103/0972-124x.118334.

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Hurst, John R. "Microbial dysbiosis in bronchiectasis." Lancet Respiratory Medicine 2, no. 12 (December 2014): 945–47. http://dx.doi.org/10.1016/s2213-2600(14)70223-1.

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Payne, M. A., A. Hashim, A. Alsam, S. Joseph, J. Aduse-Opoku, W. G. Wade, and M. A. Curtis. "Horizontal and Vertical Transfer of Oral Microbial Dysbiosis and Periodontal Disease." Journal of Dental Research 98, no. 13 (September 27, 2019): 1503–10. http://dx.doi.org/10.1177/0022034519877150.

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One of the hallmark features of destructive periodontal disease, well documented over the last 50 y, is a change to the quantitative and qualitative composition of the associated microbiology. These alterations are now generally viewed as transformational shifts of the microbial populations associated with health leading to the emergence of bacterial species, which are only present in low abundance in health and a proportionate decrease in the abundance of others. The role of this dysbiosis of the health associated microbiota in the development of disease remains controversial: is this altered microbiology the driving agent of disease or merely a consequence of the altered environmental conditions that invariably accompany destructive disease? In this work, we aimed to address this controversy through controlled transmission experiments in the mouse in which a dysbiotic oral microbiome was transferred either horizontally or vertically into healthy recipient mice. The results of these murine studies demonstrate conclusively that natural transfer of the dysbiotic oral microbiome from a periodontally diseased individual into a healthy individual will lead to establishment of the dysbiotic community in the recipient and concomitant transmission of the disease phenotype. The inherent resilience of the dysbiotic microbial community structure in diseased animals was further demonstrated by analysis of the effects of antibiotic therapy on periodontally diseased mice. Although antibiotic treatment led to a reversal of dysbiosis of the oral microbiome, in terms of both microbial load and community structure, dysbiosis of the microbiome was reestablished following cessation of therapy. Collectively, these data suggest that an oral dysbiotic microbial community structure is stable to transfer and can act in a similar manner to a conventional transmissible infectious disease agent with concomitant effects on pathology. These findings have implications to our understanding of the role of microbial dysbiosis in the development and progression of human periodontal disease.
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Vemuri, Ravichandra, Alistaire Ruggiero, Jordyn M. Whitfield, Greg O. Dugan, J. Mark Cline, Masha R. Block, Hao Guo, and Kylie Kavanagh. "Hypertension promotes microbial translocation and dysbiotic shifts in the fecal microbiome of nonhuman primates." American Journal of Physiology-Heart and Circulatory Physiology 322, no. 3 (March 1, 2022): H474—H485. http://dx.doi.org/10.1152/ajpheart.00530.2021.

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Hypertension specifically had detrimental effects on microbial translocation when age and metabolic syndrome criteria were evaluated as drivers of cardiovascular disease in a relevant nonhuman primate model. Intestinal barrier function exponentially decayed over time with chronic hypertension, and microbial translocation was confirmed by detection of more microbial genes in regional draining lymph nodes. Chronic hypertension resulted in fecal microbial dysbiosis and elevations of the biomarker NT-proBNP. This study provides insights on the barrier dysfunction, dysbiosis, and hypertension in controlled studies of nonhuman primates. Our study includes a longitudinal component comparing naturally occurring hypertensive to normotensive primates to confirm microbial translocation and dysbiotic microbiome development. Hypertension is an underappreciated driver of subclinical endotoxemia that can drive chronic inflammatory diseases
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Parida, Sheetal, and Dipali Sharma. "Microbial Alterations and Risk Factors of Breast Cancer: Connections and Mechanistic Insights." Cells 9, no. 5 (April 28, 2020): 1091. http://dx.doi.org/10.3390/cells9051091.

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Breast cancer-related mortality remains high worldwide, despite tremendous advances in diagnostics and therapeutics; hence, the quest for better strategies for disease management, as well as the identification of modifiable risk factors, continues. With recent leaps in genomic technologies, microbiota have emerged as major players in most cancers, including breast cancer. Interestingly, microbial alterations have been observed with some of the established risk factors of breast cancer, such as obesity, aging and periodontal disease. Higher levels of estrogen, a risk factor for breast cancer that cross-talks with other risk factors such as alcohol intake, obesity, parity, breastfeeding, early menarche and late menopause, are also modulated by microbial dysbiosis. In this review, we discuss the association between known breast cancer risk factors and altered microbiota. An important question related to microbial dysbiosis and cancer is the underlying mechanisms by which alterations in microbiota can support cancer progression. To this end, we review the involvement of microbial metabolites as effector molecules, the modulation of the metabolism of xenobiotics, the induction of systemic immune modulation, and altered responses to therapy owing to microbial dysbiosis. Given the association of breast cancer risk factors with microbial dysbiosis and the multitude of mechanisms altered by dysbiotic microbiota, an impaired microbiome is, in itself, an important risk factor.
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McHarg, Alexandra S., and Steven Leach. "The role of the gut microbiome in paediatric irritable bowel syndrome." AIMS Microbiology 8, no. 4 (2022): 454–69. http://dx.doi.org/10.3934/microbiol.2022030.

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<abstract> <p>Irritable bowel syndrome (IBS) is a common and disabling condition in children. The pathophysiology of IBS is thought to be multifactorial but remains incompletely understood. There is growing evidence implicating the gut microbiome in IBS. Intestinal dysbiosis has been demonstrated in paediatric IBS cohorts; however, no uniform or consistent pattern has been identified. The exact mechanisms by which this dysbiosis contributes to IBS symptoms remain unknown. Available evidence suggests the imbalance produces a functional dysbiosis, with altered production of gases and metabolites that interact with the intestinal wall to cause symptoms, and enrichment or depletion of certain metabolic pathways. Additional hypothesised mechanisms include increased intestinal permeability, visceral hypersensitivity and altered gastrointestinal motility; however, these remain speculative in paediatric patients, with studies limited to animal models and adult populations. Interaction between dietary components and intestinal microbiota, particularly with fermentable oligosaccharides, disaccharides, monosaccharides and polyols (FODMAPs), has drawn increasing attention. FODMAPs have been found to trigger and worsen IBS symptoms. This is thought to be related to products of their fermentation by a dysbiotic microbial population, although this remains to be proven. A low-FODMAP diet has shown promising success in ameliorating symptoms in some but not all patients. There remains much to be discovered about the role of the dysbiotic microbiome in paediatric IBS.</p> </abstract>
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Chalmers, James D. "Microbial Dysbiosis after Lung Transplantation." American Journal of Respiratory and Critical Care Medicine 194, no. 10 (November 15, 2016): 1184–86. http://dx.doi.org/10.1164/rccm.201606-1178ed.

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Molina, Nerea M., Alberto Sola-Leyva, Maria Jose Saez-Lara, Julio Plaza-Diaz, Aleksandra Tubić-Pavlović, Barbara Romero, Ana Clavero, Juan Mozas-Moreno, Juan Fontes, and Signe Altmäe. "New Opportunities for Endometrial Health by Modifying Uterine Microbial Composition: Present or Future?" Biomolecules 10, no. 4 (April 11, 2020): 593. http://dx.doi.org/10.3390/biom10040593.

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Current knowledge suggests that the uterus harbours its own microbiota, where the microbes could influence the uterine functions in health and disease; however, the core uterine microbial composition and the host-microbial relationships remain to be fully elucidated. Different studies are indicating, based on next-generation sequencing techniques, that microbial dysbiosis could be associated with several gynaecological disorders, such as endometriosis, chronic endometritis, dysfunctional menstrual bleeding, endometrial cancer, and infertility. Treatments using antibiotics and probiotics and/or prebiotics for endometrial microbial dysbiosis are being applied. Nevertheless there is no unified protocol for assessing the endometrial dysbiosis and no optimal treatment protocol for the established dysbiosis. With this review we outline the microbes (mostly bacteria) identified in the endometrial microbiome studies, the current treatments offered for bacterial dysbiosis in the clinical setting, and the future possibilities such as pro- and prebiotics and microbial transplants for modifying uterine microbial composition.
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Park, Kiwoong, Suhyeon Park, Arulkumar Nagappan, Navin Ray, Juil Kim, Sik Yoon, and Yuseok Moon. "Probiotic Escherichia coli Ameliorates Antibiotic-Associated Anxiety Responses in Mice." Nutrients 13, no. 3 (March 1, 2021): 811. http://dx.doi.org/10.3390/nu13030811.

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Despite the beneficial actions of antibiotics against bacterial infections, the use of antibiotics is a crucial etiological factor influencing microbial dysbiosis-associated adverse outcomes in human health. Based on the assumption that gut microbial dysbiosis can provoke behavioral or psychological disorders, the present study evaluated anxiety-linked behavioral changes in a mouse model of streptomycin-induced dysbiosis. Measuring anxiety-like behavior using the light–dark box and elevated plus maze tests indicated that streptomycin treatment caused acute anxiety in mice. As an intervention for dysbiosis-associated distress, the probiotic strain Escherichia coli Nissle 1917 (EcN) was evaluated for its effects on streptomycin-induced behavioral changes in mice. EcN supplementation persistently ameliorated anxiety responses in mice with streptomycin-induced dysbiosis. As an outcome of anxiety, body weight changes were marginally affected by antibiotic treatment. However, mice supplemented with EcN displayed acute retardation of body weight gain, since EcN is known to reduce food intake and increase energy expenditure. Taken together, EcN treatment prominently counteracted streptomycin-induced anxiety in mice, with the metabolically beneficial retardation of body weight gain. The present model simulates psychological disorders in antibiotic users. As a promising intervention, EcN treatment can facilitate psychological relief under conditions of dysbiotic stress by blocking the pathologic gut–brain circuit.
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Srivastava, Shivani, Archana Singh, Kumar Sandeep, and Durgavati Yadav. "Epigenetic Regulation of Gut Microbial Dysbiosis." Indian Journal of Microbiology 61, no. 2 (February 11, 2021): 125–29. http://dx.doi.org/10.1007/s12088-021-00920-y.

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Dissertations / Theses on the topic "MICROBIAL DYSBIOSIS"

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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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Ouarabi, Liza. "Analyses métagénomiques de l’écosystème microbien vaginal pour étudier sa spécificité et sa dynamique." Thesis, Lille 1, 2020. http://www.theses.fr/2020LIL1R040.

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Cette étude est la première dans son genre en Algérie. Elle a pour principal objectif la mise en évidence de la particularité de l’écosystème microbien vaginal chez les femmes algériennes saines, en âge de procréer et ménopausées. Elle a été réalisée sur une centaine d’échantillons vaginaux fournis par le service de gynécologie d’un établissement hospitalier privé (Bejaia, Algérie). Pour chaque femme, un examen clinique, un prélèvement vaginal et un dosage d'oestradiol ont été effectués. La composition microbienne a été déterminée par une analyse métagénomique ciblée des régions V1-V3 de l'ADNr 16S (bactéries) et des ITS1-ITS2 de l’ADNr 5,8 S (levures). Les résultats du séquençage d'Illumina ont été confirmés par qPCR. Un profil spécifique de la composition et de la dynamique du microbiote des femmes algériennes interrogées a été établi en type d'état communautaire (CST) basé sur les espèces dominantes de Lactobacillus. La composition des levures vaginales a également été abordée pendant la vie fertile et la ménopause. Toutes les données concernant les paramètres physiologiques des femmes ont été exploitées afin de voir le lien possible entre ces derniers et la composition du microbiote ou du mycobiote vaginal. Aucune corrélation n’a pu être établie entre les fluctuations hormonales, l’indice de masse corporelle et la composition microbienne de cette niche. Connaître la composition des communautés vaginales stables en état homéostatique est devenu un objectif médical principal pour les femmes algériennes. Des probiotiques personnalisés ainsi que des analyses d'exposome personnalisées pourraient être proposés pour une meilleure prise en charge de la dysbiose vaginale ou de la gêne à la ménopause
This study is the first of its kind in Algeria. Its main objective is to highlight the particularity of the vaginal microbial ecosystem in healthy Algerian women of childbearing age and in the menopause. It was carried out on a hundred vaginal samples provided by the gynaecology department of a private hospital establishment (Bejaia, Algeria). For each woman, a clinical examination, a vaginal sampling and a quantification of oestradiol were performed. Microbial composition was determined by targeted metagenomic analysis of the V1-V3 regions of the 16S rDNA (bacteria) and STI1-STI2 of the 5.8S rDNA (yeasts). Illumina sequencing results were confirmed by qPCR. A specific profile of the composition and dynamics of the microbiota of the Algerian interviewed women was established in Community State Type (CST) based on the dominant Lactobacillus species. The composition of vaginal yeasts was also addressed during fertile life and menopause. All data concerning the physiological parameters of women were exploited to see the possible link between these and the composition of the vaginal microbiota or mycobiota. No correlation could be established between hormonal fluctuations, body mass index and the microbial composition of this niche. Knowing the composition of stable vaginal communities in a homeostatic state has become a primary medical objective for Algerian women. Personalised probiotics as well as personalised exposome analyses could be proposed for a better management of vaginal dysbiosis or menopausal discomfort
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Faller, Lina Luise. "Comparative metagenomics to identify functional signatures in the human microbiome." Thesis, 2014. https://hdl.handle.net/2144/14310.

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The human microbiome, the complex and dynamic ecosystem that populates our body, performs essential functions such as aiding digestion and protecting us from harmful pathogens. An increasing number of diseases are found to be associated with a shift of balance - or dysbiosis - of the microbiome. However, we still know little about this delicate balance and how it depends on different microbial functions. In this thesis project, I used metagenomic sequencing data to study the variability of microbes and their functions in different areas of the human body. First, in an attempt to characterize the dysbiosis associated with periodontitis, I examined the microbial community of the oral cavity in presence and absence of this chronic inflammatory disease. Specifically, I catalogued the phylogenetic signatures composed of tetramer nucleotide frequencies and observed that the disease state occupies a much narrower region than the healthy one. This result suggests that upon onset of the disease, through host cell invasion, pathogenic bacteria may find a more consistent environment for their parasitic lifestyle. Motivated by these findings, I sought further evidence of an environment-specific use of metabolic functions in the oral and gut communities. Rather than focusing on the abundance of individual metabolic functions, I evaluated their diversity, i.e., the extent to which these functions are performed by different classes of organisms. My hypothesis was that such diversity may confer increased robustness to taxonomic variability. Using metagenomic sequencing data and NCBI's Protein Clusters database, I characterized the multiplicity of gene families associated with a given metabolic function. I found that different human body sites display different degrees of metabolic functional diversity, as assessed by Shannon entropy. For some well-studied gene functions, such as those involved in glycolytic pathways, I found entropy signatures consistent with the known degree of oxygen availability of different environmental niches. Conversely, in an unsupervised analysis, I identified functions with nontrivial entropy signatures. These results pave the way for a new way to inspect human microbiome activity, and could help understand its functional resilience and suggest ways to shift its balance towards healthy configurations.
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MENNINI, MAURIZIO. "Intestinal Microbiota in IgE-mediated Cow’s Milk Allergy: microbial dysbiosis and possible modulation through probiotics." Doctoral thesis, 2020. http://hdl.handle.net/11573/1364221.

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Objectives and study: The aim of the study was to evaluate gut microbiota (GM) in infants with cow milk allergy (CMA) compared to food-sensitized and healthy infants. Furthermore, we investigated colonization, persistence and possible effects of a probiotic mixture (B. breve M-16V (BB), B. longum subsp. longum BB536 (BL) and B. longum subsp. infantis M-63 (BI)) in the GM of allergic infants. Methods: We enrolled a total of 40 infants aged 10 to 15 months: 14 CMA patients (Group1); 12 positive IgE and negative food challenge patients (Group2); 14 healthy infants (Group3). For each patient, a stool sample was collected at enrolment (T 0 ). Group1 received probiotic twice per day (3.5×109 UFC/dose) for 30 days. Stool samples, collected at T 1 (7 days from probiotic intake), T2 (30 days from probiotic intake) and T 3 (after 60 day from probiotic discontinuation), were analysed by real-time PCR. The GM profile of groups was characterized by 16S rRNA targeted metagenomics. Data were analysed by QIIME and IBM SPSS Statistic software. Results: At baseline, BB and BL were present in the GM in the three Groups without significant differences. At T 0 , BI median concentration value was 0 in all the three groups, while after probiotics administration, RT-PCR analysis revealed a significant increase, from 0 to 6.4 x 10 1 molecules/l at T 1 (p=0.003) and 1.6 x 10 2 molecules/l at T 2 (p=0.005) with a decreased to 4.56 x 10 1 molecules/l at T 3. From basal microbiota comparison, we demonstrated that allergic patients clustered in Beta- diversity analysis (PERMANOVA test (p=0.019)) and showed a peculiar phylogenetic relatedness. At phylum level, Verrucomicrobia were higher in healthy group and gradually decreased from Group2 to Group1 (pFDR<0.05). Firmicutes resulted more abundant in Group2 and lower in Group3, while Group1 showed an intermediate level (pFDR<0.05). At genus level, Haemophilus, Actinobacillus, Prevotella and Streptococcus resulted associated to allergy, with a significant increase (p<0.05) in Group1 and less in Group2 compared to Group3. Klebsiella showed a higher abundance in Group1 but not in Group2 compared to Group3. Parabacteroides and Granulicatella were instead more abundant in Group3. During probiotic intake, there was an increase of Verrucomicrobia with a peak of abundance at T 2. Proteobacteria showed a gradually increase during probiotic intake and this increment was maintained also at T 3 . On the contrary, Actinobacteria decreased during the time-course, even if there was an increase form point T 1 to point T 2 . At genus level, probiotic intake determined an increase of Akkermansia, Prevotella and Ruminococcus. Actinomyces, Enterococcus, Streptococcus and Sutterella resulted instead diminished after probiotic intervention. Blautia increased during all the period of probiotic intake, until T 2 point, while at T 3 it started to decrease and showed a level of abundances lower than T 0 . Conclusion: GM of CMA infants is different from that of sensitized and healthy infants and BI can colonize and persist in CMA GM. Probiotic administration provoked an increase of anti-inflammatory and a decrease of pro-inflammatory bacteria. In conclusions, early infancy is a window during which gut microbiota may shape food allergy outcomes in childhood and probiotics could be a rational way to modulate it.
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Rosado, Daniela Filipa Gonçalves Martins. "To be or not to be diseased: microbial dynamics and dysbiosis in farmed European seabass and gilthead seabream." Doctoral thesis, 2021. https://hdl.handle.net/10216/136691.

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Rädecker, Nils. "Coral Bleaching – Breakdown of a Nutrient Exchange Symbiosis." Diss., 2019. http://hdl.handle.net/10754/655942.

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For millions of years, the nutrient exchange symbiosis between corals and their endosymbiotic algae has formed the foundation of the ecological success of coral reefs. Yet, in recent decades anthropogenic climate change is increasingly destabilizing this symbiosis, and thus the reefs that rely on it. High-temperature anomalies have caused mass mortality of corals due to repeated coral bleaching, the expulsion or digestion of symbionts by the host during stress. Hence, in-depth knowledge of the cellular processes of bleaching is required to conceive strategies to maintain the ecological functioning of coral reefs. In this thesis, we investigated the role of symbiotic nutrient cycling in the bleaching response of corals. For this, we examined the mechanisms that underlie the functioning of the symbiosis in a stable state and how heat stress affects these metabolic interactions during coral bleaching. Our findings reveal that the functioning of the coral – algae symbiosis depends on the resource competition between host and symbionts. In a stable state, symbiotic competition for ammonium limits nitrogen availability for the algal symbiont, thereby ensuring symbiotic carbon translocation and recycling. During heat stress, however, increased metabolic energy demand shifts host metabolism from amino acid synthesis to degradation. The resulting net release of ammonium by the host, coupled with the stimulated activity of associated nitrogen-fixing microbes, substantially increases nitrogen availability for algal symbionts. Subsequently, stimulated algal growth causes selfish retention of carbon, thereby further reducing energy availability for the host. This positive feedback loop disturbs symbiotic nutrient recycling, eventually causing the collapse of carbon translocation by the symbiont. Hence, heat stress causes shifts in metabolic interactions, which directly and indirectly destabilizes the symbiosis, and ultimately undermines the ecological benefits of hosting algal symbionts for corals. In summary, this thesis shows that integrating symbiotic nutrient cycling into our conceptual understanding of coral bleaching is likely to improve our ability to predict coral bleaching in light of environmental conditions and may ultimately help to conceive new strategies to preserve coral reef functioning.
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Garcia, Andreia Sofia Rodrigues. "Influence of uremic toxins on microbial intestinal epithelial barrier translocation in chronic kidney disease." Master's thesis, 2019. http://hdl.handle.net/10773/28406.

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Chronic kidney disease (CKD) is a general term for disorders affecting kidney structure and function. The progressive loss of renal function leads to the accumulation of toxins, the uremic toxins, normally cleared by the kidneys. It is under these circumstances that the “uremic state” is established. Recent studies relate uremic plasma to impaired intestinal barrier function and to depletion of the tight junctions (TJs) protein constituents. Within the intestinal lumen urea is hydrolyzed by microbial urease forming large quantities of ammonia, the major mediator of intestinal barrier disruption in uremic conditions, causing a depletion of the intestinal epithelial TJs proteins in CKD. When the microbial ecosystem is affected, harmful microbial species may overgrowth, as well their metabolism product, leading to an imbalance of the intestinal microbiome. Recent studies suggest that intestinal microbiome exert an influence over both the production of uremic toxins and the progression of CKD. In CKD, the impairment of the intestinal barrier function may allow the translocation of intestinal microorganisms, endotoxins, antigens and other microbial products from intestinal lumen to systemic circulation, contributing to the pathogenesis of systemic inflammation, cardiovascular risk and progress of CKD. Our main goal was to evaluate the application of two in vitro models of intestinal epithelial barrier for the study of microbial translocation and to evaluate the impact of different uremic conditions present in CKD on this microbial translocation. For that, we analyzed the effect of plasma of CKD patients and the uremic toxin urea on microbial intestinal translocation, as well as on integrity, permeability and localization and quantity of TJs proteins in the in vitro intestinal models, Caco-2 monoculture and Caco-2/HT29-MTX/Raji B triple model. The results showed that the experimental uremic conditions simulated in this study did not potentiate the microbial translocation, although interfered at some extent with the integrity and the permeability of intestinal epithelial barrier models. Microbial translocation was higher in Caco-2 monoculture than in triple model, suggesting that the triple model creates a more effective barrier and, therefore, apparently represents a more robust intestinal model of the human intestine. This study allowed to conclude that the uremic state influences the integrity of intestinal barrier, but this influence could not be directly translated in an increase in the microbial translocation through the intestinal epithelium in the in vitro models studied.
Doença renal crónica (DRC) é um termo geral para distúrbios que afetam a estrutura e a função do rim. A perda progressiva da função renal conduz à acumulação de toxinas, toxinas urémicas, normalmente excretadas pelos rins. É nessas circunstâncias que o "estado urémico" é estabelecido. Estudos recentes relacionam o plasma urémico ao dano da função da barreira intestinal e à depleção dos constituintes proteicos das junções de oclusão (JO). No lúmen intestinal, a ureia é hidrolisada pela urease microbiana, formando grandes quantidades de amónia, o principal mediador da disrupção da barreira intestinal em condições urémicas, causando uma depleção das proteínas das JO epiteliais intestinais na DRC. Quando o ecossistema microbiano é afetado, espécies microbianas prejudiciais podem crescer excessivamente, assim como os seus produtos do metabolismo, conduzindo a um desequilíbrio do microbioma intestinal. Estudos recentes sugerem que o microbioma intestinal exerce influência na produção de toxinas urémicas e na progressão da DRC. Na DRC, o dano da função da barreira intestinal pode permitir a translocação de microrganismos intestinais, endotoxinas, antigénios e outros produtos microbianos do lúmen intestinal para a circulação sistémica, contribuindo para a patogénese de inflamação sistémica, risco cardiovascular e progressão da DRC. O nosso principal objetivo foi avaliar a aplicação de dois modelos in vitro de barreira epitelial intestinal para o estudo da translocação microbiana e avaliar o impacto de diferentes condições urémicas presentes na DRC nessa translocação microbiana. Para isso, analisamos o efeito do plasma de doentes com DRC e da toxina urémica ureia na translocação intestinal microbiana, assim como na integridade, permeabilidade e localização e quantidade das proteínas das JO nos modelos intestinais in vitro, monocultura Caco-2 e modelo triplo Caco-2/HT29-MTX/Raji B. Os resultados mostraram que as condições urémicas experimentais simuladas neste estudo não potenciaram a translocação microbiana, embora tenham interferido em certa medida com a integridade e a permeabilidade dos modelos de barreira epitelial intestinal. A translocação microbiana foi maior na monocultura Caco-2 do que no modelo triplo, sugerindo que o modelo triplo cria uma barreira mais eficaz e, portanto, aparentemente representa um modelo intestinal mais robusto do intestino humano. Este estudo permitiu concluir que o estado urémico influencia a integridade da barreira intestinal, mas que essa influência pode não estar diretamente relacionada com um aumento da translocação microbiana através do epitélio intestinal nos modelos in vitro estudados.
Mestrado em Biomedicina Molecular
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Wallis, Amy. "Microbiota-Gut-Brain Interactions in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Focus on Neuropsychological Symptoms and Sex Comparisons." Thesis, 2017. https://vuir.vu.edu.au/37869/.

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Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a chronic, disabling condition with debilitating fatigue and neuroimmune symptoms. Consensus about diagnosis, pathogenesis and efficacious treatments for ME/CFS are yet to be elucidated. Advances in the understanding of microbiota-gut-brain interactions in healthy and disease states, combined with evidence of gastrointestinal symptoms and gut dysbiosis in individuals with ME/CFS has directed investigation towards the role of enteric microbiota in this condition. The body of work presented in this thesis includes five publications based on reviews and empirical research conducted over the past 3.5 years. The first review paper (Paper 1) found preliminary evidence to support the proposal that microbiota-gut-brain interactions may contribute to sleep, mood and cognitive symptoms but revealed gaps in knowledge with few empirical studies that have investigated commensal microbiota in patients with ME/CFS. Papers 2 and 3 describe the results of a correlational analyses between microbiota and ME/CFS symptoms in a cross-sectional, retrospective study of 274 ME/CFS patients. A notable finding from this study included sex-specific interactions between gut microbiota and symptom expression in ME/CFS, signaling possible sex differences in microbial function. The systematic review examining symptom and etiological overlap between D-lactic acidosis and ME/CFS in Paper 4, revealed preliminary support for the hypothesis that subclinical concentrations of D-lactate from bacterial dysbiosis may be a mechanism contributing to several ME/CFS symptoms (including fatigue, neurocognitive impairments, pain, sleep disturbances, motor disturbances, gastrointestinal abnormalities, cardiovascular, respiratory, thermostatic, and comorbid mood and behavioural disturbances). The review highlighted the gaps in knowledge without measurement of D-lactate concentrations in ME/CFS samples. Paper 5 presents the results of an open-label, repeated-measures trial examining the efficacy of a 4-week treatment (alternate weeks of Erythromycin and D-lactate free probiotic) for an overgrowth of commensal Streptococcus species in 44 adult patients with ME/CFS. Large time effects were shown including a reduction in Streptococcus count and improvement on several clinical outcomes (sleep, cognition and total symptoms) for the total sample at post intervention. Ancillary results highlighted individual variability in microbial changes and the importance of other genera with changes in Bacteroides, Bifidobacteria and Clostridium and associated with clinical changes in males. In combination, the analysis of literature and results from both cross-sectional and experimental studies substantiate the theoretical premise that microbiota and gut dysbiosis contribute to specific neuropsychological symptoms in some ME/CFS patients. Our mechanistic understanding of gut dysbiosis will be advanced by multidisciplinary investigations that include assessment of clinical symptoms, the microbiome (combined sequencing and culture techniques), metabolites, oxidative and inflammatory markers, and immune profiles that help identify possible factors contributing to, precipitating or perpetuating imbalances in microbial composition. These advances may help clarify diagnostic discrepancies and inform efficacious treatment alternatives that are responsive to individual variability.
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Book chapters on the topic "MICROBIAL DYSBIOSIS"

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Yang, Liying, Carlos Wolfgang Nossa, and Zhiheng Pei. "Microbial Dysbiosis and Esophageal Diseases." In Encyclopedia of Metagenomics, 379–84. Boston, MA: Springer US, 2015. http://dx.doi.org/10.1007/978-1-4899-7475-4_65.

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Curtis, Mike. "An introduction to microbial dysbiosis." In The Human Microbiota and Chronic Disease, 37–54. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2016. http://dx.doi.org/10.1002/9781118982907.ch2.

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Yang, Liying, Carlos Wolfgang Nossa, and Zhiheng Pei. "Microbial Dysbiosis and Esophageal Diseases." In Encyclopedia of Metagenomics, 1–7. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6418-1_65-1.

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Khan, Shaheerah, Rohita Sinha, Saurav Sarkar, Anshuman Dixit, and Samapika Routray. "Microbial Dysbiosis in Oral Cancer." In Microbes and Oral Squamous Cell Carcinoma, 95–106. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-0592-6_8.

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Manoil, Daniel, and Georgios N. Belibasakis. "Microbial Principles of Peri-Implant Infections." In Dental Implants and Oral Microbiome Dysbiosis, 13–29. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-99014-5_2.

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Dicksved, Johan, and Ben Willing. "The Role of Dysbiosis in Inflammatory Bowel Diseases." In Handbook of Molecular Microbial Ecology II, 199–205. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9781118010549.ch20.

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Montero, Eduardo, Margarita Iniesta, Silvia Roldán, Mariano Sanz, and David Herrera. "Microbial Manipulation of Dysbiosis: Prebiotics and Probiotics for the Treatment of Oral Diseases." In How Fermented Foods Feed a Healthy Gut Microbiota, 193–236. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-28737-5_9.

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Roman, Pablo, Lola Rueda-Ruzafa, Raquel Abalo, Francisca Carvajal, and Diana Cardona. "Gut Microbial Dysbiosis and Environmental Chemicals." In Reference Module in Food Science. Elsevier, 2021. http://dx.doi.org/10.1016/b978-0-12-819265-8.00044-9.

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do Nascimento, Wellinton M., Aline Machiavelli, Fabienne A. Ferreira, Thaís C. M. Sincero, Carlos R. Zárate-Bladés, and Aguinaldo R. Pinto. "Gut Microbial Dysbiosis and HIV Infection." In Reference Module in Food Science. Elsevier, 2021. http://dx.doi.org/10.1016/b978-0-12-819265-8.00054-1.

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Gasmi, Amin, Sadaf Noor, Salva Piscopo, and Sophie Berthouze. "Gut Microbial Dysbiosis and Cardiovascular Diseases." In Reference Module in Food Science. Elsevier, 2021. http://dx.doi.org/10.1016/b978-0-12-819265-8.00050-4.

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Conference papers on the topic "MICROBIAL DYSBIOSIS"

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Pollock, Jennifer, Alison Dicker, Mike Lonergan, Holly R. Keir, Alexandria H. Smith, Megan Crichton, Jeffrey T.-J. Huang, Bruce E. Miller, Ruth Tal-Singer, and James D. Chalmers. "Azurocidin-1: a marker of COPD severity and microbial dysbiosis." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.2340.

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Quiles, K., W. E. Johnson, and F. Chen. "Microbial Dysbiosis and Epithelial Dysfunction in Vitamin A-Deficient Lungs." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a3303.

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Keir, Holly Rachael, Hollian Richardson, Amy Gilmour, Daniela Alferes De Lima, Abirami Veluchamy, Chandani Hennayake, Merete B. Long, Diane Cassidy, Amelia Shoemark, and James D. Chalmers. "The Cathelicidin LL-37 and microbial dysbiosis in COPD patients receiving inhaled corticosteroids." In ERS Lung Science Conference 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/23120541.lsc-2022.185.

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Dolma, K., G. Rezonzew, T. Jilling, J. E. Blalock, A. Gaggar, N. Ambalavanan, and C. V. Lal. "Airway Microbial Dysbiosis Induced Neutrophilic Inflammation Leads to Bronchopulmonary Dysplasia-Like Phenotype in Mice." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a6032.

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Ying, Kevin, Min-Ae Song, Daniel Y. Weng, Quentin Nickerson, David Frankhouser, Pearlly S. Yan, Ralf Bundschuh, et al. "Abstract 246: Assessing microbial dysbiosis of electronic cigarettes and cigarette smokers using oral and lung microbiome." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-246.

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Galindo, Lia Oliver, Marta Malagón Rodríguez, Sara Ramió Pujol, Eva Lacosta, Mariona Serra Pagès, Sara Oduber, and Xavier Aldeguer Manté. "IDDF2022-ABS-0109 Clinical validation of a microbial stool test: towards a quantitative determination of intestinal dysbiosis." In Abstracts of the International Digestive Disease Forum (IDDF), Hong Kong, 2–4 September 2022. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2022. http://dx.doi.org/10.1136/gutjnl-2022-iddf.53.

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Weh, Katherine M., Nita H. Salzman, Amy B. Howell, Jennifer L. Clarke, Bridget A. Tripp, and Laura A. Kresty. "Abstract 5250: Cranberry proanthocyanidins reverse microbial dysbiosis and inhibit bile acid metabolism in association with esophageal cancer prevention." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-5250.

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Perea, L., H. Richardson, A. J. Dicker, E. Cant, M. Bottier, M. Shuttleworth, H. R. Keir, et al. "The Relationship Between Airway Interleukin-1 Beta, Microbial Dysbiosis and Mucus Hyperconcentration in Bronchiectasis: The EMBARC-BRIDGE Study." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a1997.

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Ying, Kevin L., Min-Ae Song, Daniel Y. Weng, Quentin A. Nickerson, Joseph P. McElroy, David Frankhouser, Pearlly S. Yan, et al. "Abstract 1231: Using oral and lung microbiome to assess microbial dysbiosis and inflammatory response to electronic cigarettes and to cigarettes." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-1231.

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Kitsios, G., H. Yang, L. Yang, S. Qin, A. Fitch, A. Fitch, X. Wang, et al. "Combined Dysbiosis in Upper and Lower Respiratory Tract Microbial Communities Is Associated with Inflammatory Host Responses and Worse Clinical Outcomes in Mechanically-Ventilated Patients." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a6213.

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