Project description:Hidradenitis suppurativa (HS) is an inflammatory skin disease with limited therapeutic options. We and others have previously identified an abnormal B cell infiltrate within HS lesional skin. We performed scRNASequencing on CD3 negative cells from inflammatory HS skin lesions, healthy control skin and matched blood to better understand infiltrating B cells amongst other immune cells within lesional skin.
Project description:Atopic dermatitis (AD) is a common pruritic dermatitis with macroscopically nonlesional skin that is often abnormal. Therefore, we used high-density oligonucleotide arrays to identify cutaneous gene transcription changes associated with early AD inflammation as potential disease control targets. Skin biopsy specimens analyzed included normal skin from five healthy nonatopic adults and both minimally lesional skin and nearby or contralateral nonlesional skin from six adult AD patients. Keywords: disease state analysis We used high-density oligonucleotide Affymetrix Human U133A GeneChip arrays to identify cutaneous gene transcription changes associated with early AD inflammation as potential disease control targets. Skin biopsy specimens analyzed included normal skin from five healthy nonatopic adults and both minimally lesional skin and nearby or contralateral nonlesional skin from six adult AD patients.
Project description:Hidradenitis suppurativa (HS) is an inflammatory skin disease with limited therapeutic options. Identifying transcriptional alterations within non-immune populations of HS lesions versus healthy controls could identify novel targets for therapy. We profiled subsets sorted as live, CD45 negative cells from biopsies of inflammatory lesions of three patients with HS and six specimens from healthy controls to determine what cell types and pathways were altered in HS inflammatory lesions.
Project description:Hidradenitis suppurativa (HS) is an inflammatory skin disease with limited therapeutic options. CD4 T Cells have been described as more inflammatory than T cells in healthy skin. To better understand alterations within the T cell compartment, we profiled CD4 Teffector cells and regulatory T cells (Treg) from inflammatory HS skin lesions and healthy control skin via scRNASequencing.
Project description:Atopic dermatitis (AD) is a common pruritic dermatitis with macroscopically nonlesional skin that is often abnormal. Therefore, we used high-density oligonucleotide arrays to identify cutaneous gene transcription changes associated with early AD inflammation as potential disease control targets. Skin biopsy specimens analyzed included normal skin from five healthy nonatopic adults and both minimally lesional skin and nearby or contralateral nonlesional skin from six adult AD patients. Keywords: disease state analysis
Project description:Hidradenitis suppurativa (HS) skin lesions are infiltrated by numerous inflammatory cell types, which may be subject to and can act upon surrounding tissue stroma and epithelium. Understanding how these networks are locally organized can help identify key nodes sustaining inflammatory and fibrotic processes.
Project description:To acquire a better understanding of the molecular pathogenesis of HS, we performed mRNA microarray studies to compare gene expression in lesional skin to healthy skin of HS patients. A significant difference was observed in mRNA expression between lesional and clinically healthy skin of HS patients.
Project description:We performed scRNA-seq analyses on patient matched lesional and nonlesional skin from viitiligo patients using the 10x genomics platform to examine different cell populations and keratinocyte states that may contribute to vitiligo disease persistence.
Project description:Purpose: To determine the transcriptional differences between lesional skin and nonlesional skin from patients with atopic dermatitis Methods: Skin biopsies of lesional and non-lesional sites on atopic dermatitis patients were obtained and stored in RNA Later. Ribosomal RNA was removed and cDNA was generated with the SMARTer kit (CloneTech) with 10 ng of total RNA per sample. Samples were sequenced to an average depth of 34 million 1x50 reads on a HiSeq3000 (Illumina). Reads were aligned to Ensembl release 76 using STAR, gene counts were determined with Subread:featureCount, and sequence performance was assessed with RSeQC.
Project description:Background: Plaque psoriasis is a chronic autoimmune disorder characterized by the development of red scaly plaques. To date psoriasis lesional skin transcriptome has been extensively studied, whereas only few proteomic studies of psoriatic skin are available. Aim: The aim of this study was to compare protein expression patterns of lesional and normally looking skin of psoriasis patients with skin of the healthy volunteers, reveal differentially expressed proteins and identify changes in cell metabolism caused by the disease. Methods: Skin samples of normally looking and lesional skin donated by psoriasis patients (n = 5) and samples of healthy skin donated by volunteers (n = 5) were analyzed by liquid chromatography-tandem mass spectrometry (LC-MS/MS). After protein identification and data processing, the set of differentially expressed proteins was subjected to protein ontology analysis to characterize changes in biological processes, cell components and molecular functions in the patients' skin compared to skin of the healthy volunteers. Results: The performed analysis identified 405 and 59 differentially expressed proteins in lesional and normally looking psoriatic skin compared to healthy control. We discovered decreased expression of KNG1, APOE, HRG, THBS1 and PLG in normally looking skin of the patients. Presumably, these changes were needed to protect the epidermis from spontaneous activation of kallikrein-kinin system and delay the following development of inflammatory response. In lesional skin, we identified several large groups of proteins with coordinated expression. Mainly, these proteins were involved in different aspects of protein and RNA metabolism, namely ATP synthesis and consumption; intracellular trafficking of membrane-bound vesicles, pre-RNA processing, translation, chaperoning and degradation in proteasomes/immunoproteasomes. Conclusion: Our findings explain the molecular basis of metabolic changes caused by disease in skin lesions, such as faster cell turnover and higher metabolic rate. They also indicate on downregulation of kallikrein-kinin system in normally looking skin of the patients that would be needed to delay exacerbation of the disease.