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The interaction between circulating complement proteins and cutaneous microvascular endothelial cells in the

Yao-Hsu Yang1, I-Jung Tsai1, Chun-Jung Chang2

  • 1Department of Pediatrics, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei, Taiwan.

Plos One
|March 12, 2015
PubMed

Insights

Complement activation, particularly via the alternative pathway, increases C3a and C5a levels in Henoch-Schönlein purpura (HSP). Elevated C5a may contribute to HSP pathogenesis by activating small vessel endothelium.

Area of Science:

  • Immunology
  • Pediatric Nephrology
  • Dermatology

Background:

  • Henoch-Schönlein purpura (HSP) commonly shows IgA and complement (C)3 deposition in dermal vessels.
  • Understanding the role of circulating complement proteins is crucial for elucidating HSP pathogenesis.

Purpose of the Study:

  • To investigate the role of circulating complement proteins in the pathogenesis of childhood HSP.

Main Methods:

  • Plasma levels of C3a, C4a, C5a, and Bb were measured using ELISA in 30 HSP patients and 30 controls.
  • Endothelial cell expression of C3aR, CD88, E-selectin, ICAM-1, C3, C5, IL-8, MCP-1, and RANTES was assessed via flow cytometry or ELISA.

Main Results:

  • HSP patients exhibited significantly higher plasma levels of C3a, C5a, and Bb during the acute phase compared to controls.
  • Acute phase plasma from HSP patients enhanced endothelial C3 and C5 production.
  • In vitro, C5a dose-dependently upregulated IL-8, MCP-1, E-selectin, and ICAM-1 expression in endothelial cells.

Conclusions:

  • Complement system activation, potentially via the alternative pathway, leads to increased C3a and C5a in HSP.
  • Elevated C5a levels may contribute to HSP pathogenesis by activating cutaneous small vessel endothelium.
Abstract

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