Downregulation of interleukin 36γ and its cleaver cathepsin G following treatment with narrow-band ultraviolet B phototherapy in psoriasis vulgaris. (19th May 2022)

• Record Type: Journal Article
• Authors: El-Kalioby, Mona; EL-Komy, Mohamed H. M.; Said, Eman R.; Amer, Marwa Ahmed; Saadi, Dina G.; Nouredin Mohammed, Faisal; Rashed, Laila A.; El Desouky, Eman D.; AlOrbani, Aya M.
• Is Part Of: Journal of dermatological treatment. Volume 33:Number 4(2022)
• Page Start: 2358
• Page End: 2363
• Publication Date: 2022-05-19
• Subjects: Psoriasis -- IL-36 -- NB-UVB -- protease; Skin -- Diseases -- Treatment -- Periodicals; Skin Diseases -- drug therapy -- Periodicals; Skin Diseases -- therapy -- Periodicals; 616.5
• DOI: 10.1080/09546634.2021.1967265
• Languages: English
• ISSNs: 0954-6634

Abstract

Abstract: Background: Growing evidence suggests the important role of IL-36 in the pathogenesis of psoriasis. Cathepsin G is a neutrophil-derived protease that can activate IL-36γ. Objective: To assess the expression of IL-36γ and cathepsin G in psoriasis and to quantify the impact of treatment with narrow-band ultraviolet B phototherapy (NB-UVB) on their levels. Methods: This case-control study involved 26 patients with moderate-severe psoriasis and 25 healthy volunteers. Psoriasis patients eligible for phototherapy received 24 NB-UVB sessions. Punch skin biopsies were obtained from all participants at recruitment and after phototherapy from patients. Real-time PCR was utilized for quantitative assessment of IL-36γ and cathepsin G expression in tissue samples. Results: The expression of IL-36γ and cathepsin G was significantly higher in psoriasis before NB-UVB therapy compared to controls ( p < .001). Both proteins decreased significantly with clinical improvement following NB-UVB therapy compared to baseline ( p < .001). However, their expression after treatment was still higher than controls ( p < .001). Conclusion: IL-36γ and cathepsin G expression is upregulated in psoriatic lesions, supporting their role as mediators of inflammation in psoriasis. Downregulation of IL-36γ and cathepsin G is a possible mechanism for psoriasis improvement after NB-UVB therapy. IL-36 and cathepsin G can be considered as therapeutic targets for psoriasis.