Skin dysbiosis and Staphylococcus aureus colonization in psoriasis | ||
| ARCADEs of MEDICINE | ||
| Article 13, Volume 3, Issue 2, October 2025, Pages 61-64 PDF (239.12 K) | ||
| Document Type: Review Articles | ||
| DOI: 10.21608/arcmed.2025.390040.1132 | ||
| Authors | ||
| Ahmed Ibrahim Darweesh* 1; mona Adel khatab2; Fatma El Zahraa Youssef1; Rania Abdelghani Mohammed3 | ||
| 1Microbiology Department, Armed Forces College of Medicine, Cairo, Egypt. | ||
| 2microbiology department, Armed forces college of medicine, Cairo, Egypt | ||
| 3Dermatology Department, Armed Forces College of Medicine, Cairo, Egypt. | ||
| Abstract | ||
| Psoriasis is a persistent inflammatory skin condition affecting 2–3% of people globally, arising from a complex interplay of genetic and environmental influences. The disease significantly diminishes quality of life for those affected. Recent research has drawn attention to the strong link between imbalances in the skin’s microbial community—especially the presence of Staphylococcus aureus—and increased psoriasis severity. Toxigenic strains of S. aureus, which produce superantigens like staphylococcal enterotoxins (SEs) and toxic shock syndrome toxin-1 (TSST-1), are known to worsen skin inflammation by triggering abnormal immune responses. This review examines how disruptions in the skin microbiome and colonization by S. aureus contribute to the development and progression of psoriasis. Conclusion: This review highlights the important connection between an imbalanced skin microbiome and the presence of superantigen-producing Staphylococcus aureus strains, which are linked to more severe cases of psoriasis. By addressing these microbial imbalances, we may unlock new treatment options that offer real hope for people living with psoriasis. Moving forward, deeper research into how these microbes affect the immune system will be key to creating personalized therapies that not only control symptoms but also enhance patients’ overall quality of life. | ||
| Keywords | ||
| Colonization; Dysbiosis; Psoriasis; Staphylococcus aureus; Superantigen | ||
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