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ABSTRACT: The human skin microbiome in ichthyosis vulgaris

PROVIDER: PRJEB11661 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR1110600.fastq.gz	Fastqsanger.gz
	ERR1110610.fastq.gz	Fastqsanger.gz
	ERR1110620.fastq.gz	Fastqsanger.gz
	ERR1110601.fastq.gz	Fastqsanger.gz
	ERR1110611.fastq.gz	Fastqsanger.gz

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Human gene 1.0 ST AD/IV Gene expression

Project description:Comparison of gene expression in atopic dermatitis (AD) and ichthyosis vulgaris (IV) patients skin compared to healthy control skin depending on filaggrin(FLG) genotype

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Project description:Ichthyosis Curth–Macklin is a rare genetic disorder that is clinically characterized by severe palmoplantar keratoderma. We have described previously a severe familial phenotype caused by a novel mutation in the KRT1 gene. In this study, we analyzed the skin of one patient using gene expression microarrays. We used microarrays to study the differences of gene expression between normal skin and skin affected by Ichthyosis Curth-Macklin

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Ichthyosis molecular fingerprinting shows profound Th17-skewing and a unique barrier genomic signature

Project description:The purpose of this study was to analyze the genomic signatures and profiles of skin from ichthyosis (various subtypes) vs. healthy patients. The analysis strategy was to study differentially expressed genes common to the ichthyosis shared phenotype, as well as individual ichthyosis subtypes, and compare and contrast to the genomic profiles of atopic dermatitis and psoriasis.

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Epidermal barrier impairment predisposes for excessive growth of the allergy-associated yeast Malassezia on murine skin

Project description:The skin barrier is vital for protection against environmental threats including insults caused by skin-resident microbes. Dysregulation of this barrier is a hallmark of atopic dermatitis (AD) and ichthyosis, with variable consequences for host immune control of colonizing commensals and opportunistic pathogens. While Malassezia is the most abundant commensal fungus of the skin, little is known about the host control of this fungus in inflammatory skin diseases. Here we show that in barrier-impaired skin, Malassezia acquires enhanced fitness and overt growth properties. By using four distinct and complementary murine models of atopic dermatitis and ichthyosis we provide evidence that structural and metabolic changes in the dysfunctional epidermal barrier environment provide increased accessibility and an altered lipid profile, to which the lipid-dependent yeast adapts for enhanced nutrient assimilation. These findings reveal fundamental insights into the implication of the mycobiota in the pathogenesis of common skin barrier disorders.

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Expression data from adult mouse epidermis upon tamoxifen induced inactivation of Alox12b

Project description:Autosomal recessive congenital ichthyoses (ARCI) are a group of non-syndromic congenital keratinization disorders including harlequin ichthyosis, lamellar ichthyosis, and congenital ichthyosiform erythroderma with a total prevalence of 1:200,000. Affected individuals who are often born as collodion babies present with generalized scaling of the skin. This reflects a physical compensation for the defective cutaneous permeability barrier underlying all ichthyoses. Inactivity of 12R-lipoxygenase (12R-LOX) is a frequent cause of ARCI. Epidermis-specific conditional knockout of Alox12b encoding 12R-LOX was established in mice using the Cre-Lox system. Tamoxifen-induced Alox12b inactivation in mouse skin caused an ichthyosis-like phenotype. We used microarray to compare the gene expression profile in the epidermis of mice after tamoxifen induced Alox12b inactivation with that of control animals. Inactivation of Alox12b was associated with the upregulation of genes involved in keratinization, cholesterol biosynthesis, and Fc-epsilon receptor signaling.

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Transcriptional profiling unravels enhanced xenobiotic metabolism in the skin of patients with atopic dermatitis but not with ichthyosis vulgaris

Project description:Previous transcriptome analyses confirmed the major role of immunological and skin barrier abnormalities in atopic dermatitis (AD). We here aimed at identifying novel pathogenic pathways involved in AD by comparing AD patients stratified for filaggrin (FLG) mutations not only to healthy donors but also to patients with ichthyosis vulgaris (IV). We applied single-molecule direct RNA-sequencing to analyze the whole transcriptome of nonlesional skin. Six hundred and one genes (478 up-regulated and 123 down-regulated by greater than 2-fold) were differentially expressed when all AD patients were compared to healthy donors. Expression of genes involved in RNA/protein synthesis, RNA splicing, and ATP synthesis was enhanced. Interestingly, genes involved in cell death, response to oxidative stress, DNA damage/repair and xenobiotic metabolism were largely enriched. Two hundred and thirty-seven genes (216 up-regulated and 21 down-regulated by greater than 2-fold) were altered in the skin of IV patients when compared to healthy donors. Remarkably, enhancement of xenobiotic metabolism was only detected in AD skin. Moreover, increased expression of genes encoding for keratinocyte cross-linking (SPRR2) and S100 proteins characterizes the skin of patients with AD flare when compared to patients without. We did not find significant differences in gene profiling between AD patients with and without FLG mutations.This work reveals new putative pathogenic pathways related to xenobiotic metabolisms involved in AD.

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Patients with Congenital Ichthyosis and TGM1 Mutations Overexpress Other ARCI Genes in the Skin: Part of a Barrier Repair Response?

Project description:Autosomal recessive congenital ichthyosis (ARCI) is a heterogeneous group of monogenic skin disorders caused by mutations in any of >10 different genes, many of which are involved in epidermal synthesis of ω-O-acylceramides (acylCer), an essential precursor of the corneocyte lipid envelope that is also dependent on transglutaminase-1 for normal skin barrier formation. We hypothesized that inactivating TGM1 mutations, the most common cause of ARCI, might lead to a compensatory overexpression of transcripts involved in barrier repair, including ARCI-causing genes. Using microarray we examined the global mRNA expression profile in skin biopsies from five ARCI-patients with TGM1 mutations and four healthy controls. There were a total of 602 differentially expressed genes (adjusted P<0.05). Gene ontology analysis showed enrichment of mRNA encoding proteins associated with biological pathways mainly involved in keratinocyte differentiation and adaptive/innate immune response. Moreover, among non-syndromic ARCI-causing genes, seven out of twelve were significantly increased (log2fold -change=0.98-2.05). Four genes causing syndromic ichthyosis and seven other genes involved in biosynthesis of fatty acyl-CoA and ceramides were also significantly affected. This study reveals upregulation of several ichthyosis-causing genes in the skin of patients with TGM1 mutations, indicating a compensatory induction of acylCer biosynthesis as a part of a barrier repair mechanism.

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