Staphylococcus aureus aggravates psoriasis in human keratinocytes with the assistance of IL-17A and TNF- α, along with a contribution from genes associated with skin cutaneous melanoma

Articles in Press

Document Type : Original article

Authors

1 Department of Anatomy, Al-Batool College of Medicine, University of Mosul, Iraq

2 Department of Biology, Tikrit University, Iraq

10.22099/mbrc.2025.54205.2207

Abstract

Psoriasis patients were 4- 5 times more likely to have S. aureus colonize their skin. Psoriasis is caused by staphylococcal infection-induced keratinocyte death, which is maintained by elevated cytokine production of TNF-α and IFN-γ. The study sought to determine the association between the influence of gene expression of certain genes in psoriasis infections in the presence of S. aureus and their effect in Skin Cutaneous Melanoma infections. GEO with accession number (GSE207390) was used to acquire the data. The microarray test was used to perform this investigation. Six sets of keratinocytes, IL-17A, and TNF-α were cultivated together. Several kinds of bioinformatics tools were employed to fulfill the study's objective. Gene hub analysis of 34284 genes was scanned. Six genes demonstrated high expression rates were expressed during the metastatic stage: CCL27, IL19, PAPPA2, UHRF1, IFNAR2, and GLS2. IFNAR2 and UHRF1 had the highest levels of expression. The expression of the COL4A4 gene rose in response to sun exposure, but the expression of the other genes remained same. The existence of cytokine groups with S. aureus in keratinocytes influences the expression difference compared to the other groups. This work adds to our understanding of the molecular alterations that occur in the epidermis of psoriasis patients, as well as their relationship to comorbidities.

Keywords

Molecular Biology Research Communications

Articles in Press, Accepted Manuscript
Available Online from 16 March 2026

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