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

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.