The Distinctive Immunologic Pathogenesis Differentiates Atopic Comorbidity Status in Prurigo Nodularis
- Author:
Howard CHU
1
;
Wan Jin KIM
;
Su Min KIM
;
Seo Hyeong KIM
;
Ji Hye KIM
;
Kelun ZHANG
;
Hye Li KIM
;
Ryeo Won KIM
;
Kwang Hoon LEE
;
Chang Ook PARK
Author Information
1. Department of Dermatology, Severance Hospital, Cutaneous Biology Research Instiutute, Yonsei University College of Medicine , Seoul, Korea
- Publication Type:Original Article
- From:Korean Journal of Dermatology
2022;60(10):666-674
- CountryRepublic of Korea
- Language:English
-
Abstract:
Background:Prurigo nodularis (PN) is a chronic pruritic skin disorder with a large number of hyperkeratotic nodules. The precise mechanisms of its pathogenesis remain unknown. PN has been linked to atopic dermatitis (AD), but its association remains unclear.
Objective:We aimed to investigate the clinical, histological, and immunohistochemical characteristics of patients with PN and PN underlying AD (PN-AD).
Methods:Eight patients were recruited for PN, PN-AD, and eight normal subjects, respectively. Skin tissues were obtained from patients and healthy subjects for histological and immunohistochemical analyses.
Results:Histological examination showed increased epidermal thickness and dermal inflammatory cell counts in the PN-AD and PN groups compared to normal subjects. Immunohistochemical analyses revealed that the expression of interleukin (IL)-4, IL-13, IL-18, IL-31, IL-33, interferon (IFN)-γ, stromal-derived factor (SDF) 1-α and thymic stromal lymphopoietin (TSLP) was increased in the tissues of PN-AD and PN groups, in which the staining intensities of IL-4, IL-13, SDF1-α and TSLP in the PN-AD group were higher than those in the PN group, but the differences were not statistically significant. Conversely, the staining intensities of IL-18, IL-33 and IFN-γ were significantly higher in the PN group than those in the PN-AD group.
Conclusion:The pathogenesis of PN may differ from that of PN-AD, in which IL-18, IL-33 and IFN-γ may be associated, implying that epidermal injury is the initial cause of IL-18 and IL-33 induction, which then increases IFN-γ, resulting in the inflammatory process of PN.
