Human skin metagenome and 16S
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ABSTRACT:
PROVIDER: PRJNA1162089 | ENA |
REPOSITORIES: ENA
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Project description:Shotgun metagenomics of fecal bacterial consortium inhabiting healthy Asian children
| PRJDB4525 | ENA
Project description:Background: DOCK8 deficiency is an autosomal recessive form of hyperimmunoglobulinemia E syndrome (HIES). Severe atopic dermatitis (AD) shares with DOCK8 deficiency some clinical symptoms, including eczema, eosinophilia, and increased serum IgE levels. The deficiency of DOCK8 protein is potentially a life-threatening autosomal recessive HIES and only curable with bone marrow transplantation. Despite identified metabolomics and cytokine biomarkers, novel proteomics biomarkers need to be identified, as the connecting networks are critical to our understanding of this disease. Hence we performed serum proteomics profiling using LC-MSE SynaptG2. Method: Label-free untargeted proteomics analysis was used to identify potentially reliable, sensitive, and specific protein biomarkers in serum collected from DOCK8 (n=10), AD (n=9) patients, which were compared to ctrls (n=5). Results: From a total of 275 quantifiable proteins, binary comparisons between AD vs. Ctrl, DOCK8 vs. Ctrl, and DOCK8 vs. AD revealed 109, 105 and 85 dysregulated proteins, respectively. 24 among 85 proteins were specific potential biomarkers among the DOCK8 and AD groups. The sensitivity and specificity of few proteins like Claspin, Immunoglobulin kappa and heavy, complement components as potential biomarkers to distinguish between DOCK8 and AD patients were evaluated using the receiver operating characteristic curve. DOCK8 deficiency and AD groups' profiling revealed a shared role of ERK1/2 among the commonly dysregulated proteins. Conclusion: In this study, we have identified potential proteomics biomarkers and profile to distinguish between DOCK8 and AD, with possible diagnostic and therapeutic applications to help create effective interventions for managing these diseases. Further studies to confirm these associations in prospective cohorts are warranted.
2022-05-17 | PXD029052 | Pride
Project description:In this study we developed metaproteomics based methods for quantifying taxonomic composition of microbiomes (microbial communities). We also compared metaproteomics based quantification to other quantification methods, namely metagenomics and 16S rRNA gene amplicon sequencing. The metagenomic and 16S rRNA data can be found in the European Nucleotide Archive (Study number: PRJEB19901). For the method development and comparison of the methods we analyzed three types of mock communities with all three methods. The communities contain between 28 to 32 species and strains of bacteria, archaea, eukaryotes and bacteriophage. For each community type 4 biological replicate communities were generated. All four replicates were analyzed by 16S rRNA sequencing and metaproteomics. Three replicates of each community type were analyzed with metagenomics. The "C" type communities have same cell/phage particle number for all community members (C1 to C4). The "P" type communities have the same protein content for all community members (P1 to P4). The "U" (UNEVEN) type communities cover a large range of protein amounts and cell numbers (U1 to U4). We also generated proteomic data for four pure cultures to test the specificity of the protein inference method. This data is also included in this submission.
2017-05-12 | PXD006118 | Pride
Project description:To examine the effect of DOCK8 deficiency on helper T cell differentiation, we employed microarray expression profiling and found that 850 genes were expressed at higher levels in Dock8–/– AND CD4+ T cells than Dock8+/– controls after antigen stimulation.
2016-12-01 | GSE75686 | GEO
Project description:Genome wide DNA methylation profiling of isolated monocyte samples from healthy Kenyan children, the same children during an episode of acute malaria, healthy Kenyan adults, and healthy adults from the United States. The Illumina Infinium MethylationEPIC BeadChip microarray was used to obtain DNA methylation profiles across approximately 860,000 CpGs in negatively selected monocyte samples. Samples included monocytes from 8 children from western Kenya obtained while healthy and matching samples from the same 8 Kenyan children obtained during an episode of acute uncomplicated Plasmodium falciparum malaria, 8 healthy malaria-immune adults from western Kenya, and 8 healthy malaria-naive adults from the US. Abstract -- Background: Age-related changes in adaptive and innate immune cells have been associated with a decline in effective immunity and chronic, low-grade inflammation. Epigenetic, transcriptional, and functional changes in monocytes occur with aging, though most studies to date have focused on differences between young adults and the elderly in populations with European ancestry; few data exist regarding changes that occur in circulating monocytes during the first few decades of life or in African populations. We analyzed DNA methylation profiles, cytokine production, and inflammatory gene expression profiles in monocytes from young adults and children from western Kenya. Results: We identified several hypo- and hyper-methylated CpG sites in monocytes from Kenyan young adults vs. children that replicated findings in the current literature of differential DNA methylation in monocytes from elderly persons vs. young adults across diverse populations. Differentially methylated CpG sites were also noted in gene regions important to inflammation and innate immune responses. Monocytes from Kenyan young adults vs. children displayed increased production of IL-8, IL-10, and IL-12p70 in response to TLR4 and TLR2/1 stimulation as well as distinct inflammatory gene expression profiles. Conclusions: These findings complement previous reports of age-related methylation changes in isolated monocytes and provide novel insights into the role of age-associated changes in innate immune functions.
2021-03-11 | GSE157611 | GEO
Project description:Skin microbiome of six healthy Japanese adults.
| PRJDB15042 | ENA
Project description:COVit - Nicotinamide Placebo Study - 16S and shotgun metagenomics
| PRJEB61276 | ENA
Project description:Characterisation of the forehead and armpit skin microbiome of healthy individuals using shotgun metagenomics and 16S rRNA gene sequencing
| PRJEB80549 | ENA
Project description:Dedicator of cytokinesis 8 (DOCK8) deficiency is an autosomal-recessive immunodeficiency disorder that manifests with hyper-IgE syndrome and susceptibility to viral, bacterial, fungal, and parasitic infections as well as malignancy, atopy, and autoimmunity. Up to two-thirds of DOCK8-deficient patients develop chronic mucocutaneous candidiasis (CMC), yet the mechanistic basis for this susceptibility remains elusive. Here, we utilized a mouse model of oral candidiasis to investigate the cellular and molecular mechanisms that drive CMC susceptibility in DOCK8 deficiency. We demonstrate that DOCK8 promotes mucosal fungal clearance via the induction of protective type-17 immune responses. Mechanistically, in the absence of DOCK8, the accumulation of IL-17+ and IL-22+ TCRαβ T cells, γδ T cells, and innate lymphoid cells (ILCs) was markedly decreased in the oral mucosa, driven by increased apoptotic cell death, not impaired cell proliferation or recruitment from the blood. Unexpectedly, DOCK8 was required for the cell-intrinsic acquisition of a type-17 phenotype only in oral mucosal γδ T cells, but not in TCRαβ T cells or ILCs in vivo. Concordantly, mice with conditional DOCK8 deletion in all RORγt-expressing IL-17-producing lymphoid cells, but not in CD4+ T cells alone, were susceptible to oral candidiasis. Moreover, prophylactic administration of the gc family cytokine IL-7 rescued lymphocyte apoptosis, increased the number of IL-17+ and IL-22+ cells, and promoted fungal clearance in DOCK8-deficient mice. Thus, we show that mucosal candidiasis in DOCK8 deficiency is driven by multicellular defects in lymphocyte survival and accumulation resulting in impaired type-17 immunity. IL-7 immunotherapy boosts mucosal type-17 responses and ameliorates fungal susceptibility.
2026-03-27 | GSE293085 | GEO
Project description:Skin shotgun metagenomics in patients with GNAI2 mutations
| PRJNA1104145 | ENA