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Circulating Monocytes are Predictive and Responsive in Moderate-to-Severe Plaque Psoriasis Subjects Treated with Apremilast

ABSTRACT: Circulating Monocytes are Predictive and Responsive in Moderate-to-Severe Plaque Psoriasis Subjects Treated with Apremilast

PROVIDER: PRJNA1078849 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28035872.fastq.gz	Fastqsanger.gz
	SRR28035873.fastq.gz	Fastqsanger.gz
	SRR28035874.fastq.gz	Fastqsanger.gz
	SRR28035875.fastq.gz	Fastqsanger.gz
	SRR28035876.fastq.gz	Fastqsanger.gz

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Circulating Monocytes are Predictive and Responsive in Moderate-to-Severe Plaque Psoriasis Subjects Treated with Apremilast

Project description:Monocytes play a critical role in the inflammation associated with psoriasis, and their abnormalities have been reported as biomarkers of cardiovascular event risk, a psoriasis comorbidity. Monocytic cells in chronic inflammatory disorders express elevated levels of cAMP phosphodiesterase. Restoring cAMP levels using the oral cAMP phosphodiesterase-4 inhibitor, apremilast, improves clinical outcomes for a subset of psoriasis patients. We asked whether aberrant monocyte subsets or transcriptomic pathways can function as biomarkers of psoriasis endotypes that can predict enhanced clinical responses to cAMP phosphodiesterase inhibition. A 16-week open-label study of 22 patients with monocyte flow cytometric and transcriptomic analysis was performed. Subjects with elevated hyper-adhesive monocyte doublets at baseline were more likely to be responders to apremilast (p< 0.0001); 82% of subjects with elevated hyper-adhesive monocyte doublets achieved 50% reduction in PASI (PASI50) compared to 46% in those without elevated doublets. We observed a significant reduction in hyper-adhesive monocyte-containing doublets and monocyte-platelet aggregates, suggesting an effect of apremilast on the adhesiveness of blood monocytes during chronic inflammation. Monocyte differentially-expressed gene transcripts predictive of clinical response uncovered pharmaco-endotypes with distinct patterns of nucleotide metabolism, energetics, and differentiation. Further study to understand the basis of drug responsiveness, and to develop an apremilast psoriasis treatment algorithm using monocyte refined gene expression is required to validate and become practical in clinical use, offering patients a test that personalizes their likelihood of clinical response.

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Project description:Inverse and erythrodermic psoriasis are rare subtypes of psoriasis. Whereas the former is characterized by shiny erythematous non-scaly plaques in the body folds, the latter has widespread redness with fine scale, covering over 80% of the body-surface area, and can be life-threatening. Both are considered to be clinical subtypes of chronic plaque psoriasis, and often co-exist or evolve from plaque psoriasis (Boyd and Menter, 1989; Omland and Gniadecki, 2015), but the pathogenic mechanisms involved are unknown, and current treatments are frequently unsatisfactory. To assess shared and unique processes between chronic plaque, inverse, and erythrodermic psoriasis we analyzed archived formalin-fixed paraffin-embedded biopsies of clinically and histologically confirmed chronic plaque (n=12), inverse (n=40) and erythrodermic psoriasis cases (n=30) and healthy control skin (n=20) using Affymetrix ST 2.1 Arrays. Compared with healthy skin, psoriatic plaque lesions yielded 2450 differentially expressed genes (DEGs) (FDR, p<0.05), inverse psoriasis lesions yielded 408 DEGs (FDR, p<0.05) and erythrodermic psoriasis lesions yielded 447 DEGs (FDR, p<0.05). In total 294 genes were found to be shared among the three disease subtypes (FDR, p<0.05). While the overlap only accounted for 12% of the DEGs in chronic plaque psoriasis, it accounted for 66% and 72% of DEGs in erythrodermic and inverse psoriasis respectively.

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Project description:Scalp psoriasis shows a variable clinical spectrum and in many cases poses a great therapeutic challenge. However, it remains unknown whether the immune response of scalp psoriasis differs from understood pathomechanisms of psoriasis on other skin areas. We sought to determine the cellular and mollecular phenotype of scalp psoriasis by performing a comparative analysis of scalp vs skin using lesional and nonlesional samples from 20 Caucasian subjects with untreated moderate to severe psoriasis and significant scalp involvement, and 10 control subjects without psoriasis. Our results suggest that even in the scalp psoriasis is a disease of the inter-follicular skin. The immune mechanisms that mediate scalp psoriasis were found to be similar to those involved in skin psoriasis. However, the magnitude of dysregulation, number of differentially expressed genes, and enrichment of the psoriatic genomic fingerprinting were more prominent in skin lesions. Furthermore, the scalp transcriptome showed increased modulation of several gene-sets, particularly those induced by interferon-gamma, compared with skin psoriasis which was mainly associated with activation of TNFâµ/L-17/IL-22-induced keratinocyte response genes. We also detected differences in expression of gene-sets involving negative regulation, epigenetic regulation, epidermal differentiation, and dendritic cell or Th1/Th17/Th22-related T-cell processes. To define the transcriptomic profile of scalp skin, punch biopsies (6 mm diameter) were obtained from 20 Caucasian patients with untreated moderate to severe psoriasis with significative scalp involvement and 10 control subjects without psoriasis (N). Lesional (LS) samples were isolated from the infiltrated border of a plaque of psoriasis. Non lesional (NL) samples were taken from scalp areas with no visible psoriasis between the infiltrated plaques.

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Expression data from skin biopsy samples from patients with moderate-to-severe psoriasis

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