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Sökning: WFRF:(Debelius Justine W)

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1.
  • Debelius, Justine W, et al. (författare)
  • A comparison of approaches to scaffolding multiple regions along the 16S rRNA gene for improved resolution
  • 2021
  • Ingår i: BiorXiv. - : Cold Spring Harbor Laboratory.
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
    • MotivationFull length, high resolution 16s rRNA marker gene sequencing has been challenging historically. Short amplicons provide high accuracy reads with widely available equipment, at the cost of taxonomic resolution. One recent proposal has been to reconstruct multiple amplicons along the full-length marker gene, however no barcode-free computationally tractable approach for this is available. To address this gap, we present Sidle (SMURF Implementation Done to acceLerate Efficiency), an implementation of the Short MUltiple Reads Framework algorithm with a novel tree building approach to reconstruct rRNA genes from individually amplified regions.ResultsUsing simulated and real data, we compared Sidle to two other approaches of leveraging multiple gene region data. We found that Sidle had the least bias in non-phylogenetic alpha diversity, feature-based measures of beta diversity, and the reconstruction of individual clades. With a curated database, Sidle also provided the most precise species-level resolution.Availability and ImplementationSidle is available under a BSD 3 license from https://github.com/jwdebelius/q2-sidle
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2.
  • Gudnadottir, Unnur, et al. (författare)
  • The vaginal microbiome and the risk of preterm birth : a systematic review and network meta-analysis
  • 2022
  • Ingår i: Scientific Reports. - : Springer Nature. - 2045-2322. ; 12
  • Tidskriftsartikel (refereegranskat)abstract
    • Preterm birth is a major cause of neonatal morbidity and mortality worldwide. Increasing evidence links the vaginal microbiome to the risk of spontaneous preterm labour that leads to preterm birth. The aim of this systematic review and network meta-analysis was to investigate the association between the vaginal microbiome, defined as community state types (CSTs, i.e. dominance of specific lactobacilli spp, or not (low-lactobacilli)), and the risk of preterm birth. Systematic review using PubMed, Web of Science, Embase and Cochrane library was performed. Longitudinal studies using culture-independent methods categorizing the vaginal microbiome in at least three different CSTs to assess the risk of preterm birth were included. A (network) meta-analysis was conducted, presenting pooled odds ratios (OR) and 95% confidence intervals (CI); and weighted proportions and 95% CI. All 17 studies were published between 2014 and 2021 and included 38-539 pregnancies and 8-107 preterm births. Women presenting with "low-lactobacilli" vaginal microbiome were at increased risk (OR 1.69, 95% CI 1.15-2.49) for delivering preterm compared to Lactobacillus crispatus dominant women. Our network meta-analysis supports the microbiome being predictive of preterm birth, where low abundance of lactobacilli is associated with the highest risk, and L. crispatus dominance the lowest.
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3.
  • Chen, Yufeng, et al. (författare)
  • Oral fungal profiling and risk of nasopharyngeal carcinoma : a population-based case-control study
  • 2023
  • Ingår i: EBioMedicine. - 2352-3964. ; 96
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Dysbiosis of the oral mycobiome has been linked to some diseases, including cancers. However, the role of oral fungal communities in nasopharyngeal carcinoma (NPC) carcinogenesis has not previously been investigated.METHODS: We characterized the oral salivary fungal mycobiome in 476 untreated incident NPC patients and 537 population-based controls using fungal internal transcribed spacer (ITS)-2 sequencing. The relationship between oral fungal mycobiome and the risk of NPC was assessed through bioinformatic and biostatistical analyses.FINDINGS: We found that lower fungal alpha diversity was associated with an increased odds of NPC [lower vs. higher: observed features (adjusted odds ratio [OR] = 5.81, 95% confidence interval [CI] = 3.60-9.38); Simpson diversity (1.53, 1.03-2.29); Shannon diversity (2.03, 1.35-3.04)]. We also observed a significant difference in global fungal community patterns between cases and controls based on Bray-Curtis dissimilarity (P < 0.001). Carriage of oral fungal species, specifically, Saccharomyces cerevisiae, Candida tropicalis, Lodderomyces elongisporus, Candida albicans, and Fusarium poae, was associated with significantly higher odds of NPC, with ORs ranging from 1.56 to 4.66. Individuals with both low fungal and low bacterial alpha diversity had a profoundly elevated risk of NPC.INTERPRETATION: Our results suggest that dysbiosis in the oral mycobiome, characterized by a loss of fungal community diversity and overgrowth of several fungal organisms, is associated with a substantially increased risk of NPC.FUNDING: This work was funded by the US National Institutes of Health, the Swedish Research Council, the High-level Talents Research Start-up Project of Fujian Medical University, and the China Scholarship Council.
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4.
  • Sampson, Timothy R., et al. (författare)
  • A gut bacterial amyloid promotes α-synuclein aggregation and motor impairment in mice
  • 2020
  • Ingår i: eLife. - 2050-084X. ; 9
  • Tidskriftsartikel (refereegranskat)abstract
    • Amyloids are a class of protein with unique self-aggregation properties, and their aberrant accumulation can lead to cellular dysfunctions associated with neurodegenerative diseases. While genetic and environmental factors can influence amyloid formation, molecular triggers and/or facilitators are not well defined. Growing evidence suggests that non-identical amyloid proteins may accelerate reciprocal amyloid aggregation in a prion-like fashion. While humans encode ~30 amyloidogenic proteins, the gut microbiome also produces functional amyloids. For example, curli are cell surface amyloid proteins abundantly expressed by certain gut bacteria. In mice overexpressing the human amyloid α-synuclein (αSyn), we reveal that colonization with curli-producing Escherichia coli promotes αSyn pathology in the gut and the brain. Curli expression is required for E. coli to exacerbate αSyn-induced behavioral deficits, including intestinal and motor impairments. Purified curli subunits accelerate αSyn aggregation in biochemical assays, while oral treatment of mice with a gut-restricted amyloid inhibitor prevents curli-mediated acceleration of pathology and behavioral abnormalities. We propose that exposure to microbial amyloids in the gastrointestinal tract can accelerate αSyn aggregation and disease in the gut and the brain.
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5.
  • Sampson, Timothy R, et al. (författare)
  • Gut Microbiota Regulate Motor Deficits and Neuroinflammation in a Model of Parkinson's Disease.
  • 2016
  • Ingår i: Cell. - : Elsevier BV. - 0092-8674 .- 1097-4172. ; 167:6, s. 1469-1480.e12
  • Tidskriftsartikel (refereegranskat)abstract
    • The intestinal microbiota influence neurodevelopment, modulate behavior, and contribute to neurological disorders. However, a functional link between gut bacteria and neurodegenerative diseases remains unexplored. Synucleinopathies are characterized by aggregation of the protein α-synuclein (αSyn), often resulting in motor dysfunction as exemplified by Parkinson's disease (PD). Using mice that overexpress αSyn, we report herein that gut microbiota are required for motor deficits, microglia activation, and αSyn pathology. Antibiotic treatment ameliorates, while microbial re-colonization promotes, pathophysiology in adult animals, suggesting that postnatal signaling between the gut and the brain modulates disease. Indeed, oral administration of specific microbial metabolites to germ-free mice promotes neuroinflammation and motor symptoms. Remarkably, colonization of αSyn-overexpressing mice with microbiota from PD-affected patients enhances physical impairments compared to microbiota transplants from healthy human donors. These findings reveal that gut bacteria regulate movement disorders in mice and suggest that alterations in the human microbiome represent a risk factor for PD.
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