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CCL5, CXCL16, and CX3CL1 are associated with Henoch-Schonlein purpura

Tao Chen1, Zai-Pei Guo, Xiao-Yan Jiao

  • 1Department of Dermatovenereology, West China Hospital of Sichuan University, Chengdu, China.

Archives of Dermatological Research
|June 4, 2011
PubMed

Insights

Chemokines like CCL5, CXCL16, and CX3CL1 are elevated in Henoch-Schonlein purpura (HSP) patients and contribute to vascular inflammation. Active HSP sera induce chemokine production in endothelial cells via NF-κB and ERK pathways.

Area of Science:

  • Vascular Biology
  • Immunology
  • Rheumatology

Background:

  • Chemokines play a role in vascular inflammation.
  • Limited data exists on chemokine involvement in Henoch-Schonlein purpura (HSP).

Purpose of the Study:

  • To investigate serum levels of CCL5, CXCL16, and CX3CL1 in HSP patients.
  • To assess the effect of HSP patient sera on chemokine production in human dermal microvascular endothelial cells (HMEC-1).

Main Methods:

  • Enzyme-linked immunosorbent assay (ELISA) to measure serum chemokine levels.
  • Treatment of HMEC-1 cells with sera from HSP patients, acute spontaneous urticaria patients, and controls.
  • Analysis of chemokine mRNA and protein levels, cell migration, and intracellular signaling pathways (NF-κB, ERK).

Main Results:

  • Serum CCL5, CXCL16, and CX3CL1 levels were elevated in acute HSP and correlated with disease severity.
  • Sera from active HSP patients induced chemokine production in HMEC-1 cells.
  • HSP sera-stimulated HMEC-1 cells enhanced leukocyte migration and activated NF-κB and ERK signaling pathways.

Conclusions:

  • CCL5, CXCL16, and CX3CL1 are implicated in the pathogenesis of HSP.
  • Factors in active HSP sera induce inflammatory responses in endothelial cells, promoting chemokine production via NF-κB and ERK pathways.

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