Clinical and Proteomic Profiling of Inflammatory Mediators in Henoch-Schönlein Purpura: Oncostatin M as a Key Cytokine Associated with Disease Severity.

Abstract

Introduction: Henoch-Schönlein purpura (HSP) is a systemic vessel vasculitis characterized by IgA- and complement-mediated vascular injuries. However, the precise mechanisms underlying disease progression and severity remain unclear. This study aimed to identify inflammation-related proteins and pathways associated with HSP and disease severity.

Methods: Plasma samples from 10 patients with HSP and 10 healthy controls (HC) were analyzed using the Olink inflammation panel. Patients were categorized into simple purpura (HSP_S) and complex purpura (HSP_C) groups based on clinical manifestations. Clinical and laboratory characteristics were also collected for analysis.

Results: Patients in HSP_C group showed significant higher level of 24-h urine protein quantification (p = 0.038). Among the 92 inflammation-related proteins analyzed, 13 were differentially expressed between patients with HSP and HC. Notably, Oncostatin M (OSM), interleukin-6 (IL-6), and transforming growth factor-α (TGF-α) were significantly elevated in HSP patients. Compared with the HSP_S group, HSP_C group exhibited increased levels of fibroblast growth factors (FGF19), glial cell line-derived neurotrophic factor, HGF, and OSM. Pathway enrichment revealed upregulation of the JAK-STAT and PI3K-Akt signaling pathways in HSP_C group, suggesting their involvement in disease severity. Protein-protein interaction analysis identified OSM, IL-6, TGF-α, and IL-18 as key inflammatory hubs, with OSM showing the strongest correlation with systemic injury.

Conclusions: This study provides novel insights into the inflammatory proteomic landscape of HSP patients, highlighting OSM as a potential biomarker of disease severity and systemic injury. The JAK-STAT and PI3K-Akt pathways may play central roles in HSP pathogenesis and represent potential therapeutic targets.