Abstract
Psoriasis is a multifactorial immune-mediated disease. The highly effective and eligible treatment for psoriasis is limited, for its specific pathogenesis is incompletely elucidated. Skin microbiota is a research hotspot in the pathogenesis of immune-mediated inflammatory skin diseases nowadays, and it may have significant involvement in the provocation or exacerbation of psoriasis with broadly applicable prospects. It is postulated that skin microbiota alternation may interplay with innate immunity such as antimicrobial peptides and Toll-like receptors to stimulate T-cell populations, resulting in immune cascade responses and ultimately psoriasis. Achieving a thorough understanding of its underlying pathogenesis is crucial. Herein, we discuss the potential immunopathogenesis of psoriasis from the aspect of skin microbiota in an attempt to yield insights for novel therapeutic and preventive modalities for psoriasis.
Highlights
Psoriasis is a chronic systemic inflammatory disease contributed by genetic, immunological, and environmental factors, with a prevalence rate of 2%–4% of the worldwide population [1]
This article describes the potential pathogenesis of psoriasis concerning how skin microbiota interplay with the host immune system, aiming at providing new insights regarding the immunopathogenesis of psoriasis
In the trial of Balci et al [58], S. aureus was cultivated from lesional skin in approximately 64% of psoriatic patients, significantly higher than about 30% from non-lesional and healthy control samples, and 60% of patients were detected with Staphylococcus enterotoxins and toxic shock syndrome toxin-1 (TSST-1)
Summary
Psoriasis is a chronic systemic inflammatory disease contributed by genetic, immunological, and environmental factors, with a prevalence rate of 2%–4% of the worldwide population [1]. Current research has put emphasis on the role of skin microbiome in immune-mediated inflammatory skin diseases, including atopic dermatitis, acne vulgaris, vitiligo, and systemic lupus erythematosus [4,5,6,7,8], yet there are certain blank regions in psoriasis. Even though the causal link between skin microbiome and psoriasis remains elusive, evolving knowledge supports its potential role interplaying on T helper cell 17 (Th17) in psoriatic patients, acting on inflammatory cells and cytokine pathways to induce immunity disorder on skin, confirmed by detection of plasma metabolism and bacterial metabolites [9]. This article describes the potential pathogenesis of psoriasis concerning how skin microbiota interplay with the host immune system, aiming at providing new insights regarding the immunopathogenesis of psoriasis. A good knowledge about their intrinsic and comprehensive interplay is certainly beneficial to form the basis of innovative treatment selection and may help revolutionize an unprecedented era of biologic therapies for psoriatic patients
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