Korean J Dermatol.  2022 Dec;60(10):666-674.

The Distinctive Immunologic Pathogenesis Differentiates Atopic Comorbidity Status in Prurigo Nodularis

• Chu H
• Kim WJ
• Kim SM
• Kim SH
• Kim JH
• Zhang K
• Kim HL
• Kim RW
• Lee KH
• Park CO

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.

Keyword

Atopic dermatitis; Cytokines; Immunohistochemistry; Prurigo