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Myeloid-related proteins 8 and 14 contribute to monosodium urate monohydrate crystal-induced inflammation in gout

Dirk Holzinger1, Nadine Nippe, Thomas Vogl

  • 1University Hospital Muenster and University Children's Hospital Muenster, Muenster, Germany.

Arthritis & Rheumatology (Hoboken, N.J.)
|January 29, 2014
PubMed
Abstract

Insights

Myeloid-related proteins (MRP-8 and MRP-14) enhance monosodium urate (MSU) crystal-induced IL-1β secretion, a key factor in gout pathogenesis. These proteins contribute to gout inflammation by acting as endogenous Toll-like receptor 4 agonists.

Area of Science:

  • Rheumatology
  • Immunology
  • Crystal-induced arthritis

Background:

  • Monosodium urate (MSU) crystal-induced interleukin-1β (IL-1β) secretion is central to gout pathogenesis.
  • MSU crystals alone do not induce IL-1β secretion, requiring costimulatory factors for priming.
  • The endogenous costimulatory factors involved in gout pathogenesis remain largely unknown.

Purpose of the Study:

  • To investigate the costimulatory properties of myeloid-related protein 8 (MRP-8) and MRP-14 in MSU crystal-induced IL-1β secretion.
  • To determine the role of MRP-8 and MRP-14 as endogenous Toll-like receptor 4 (TLR-4) agonists in gout.
  • To assess the relevance of MRP-8 and MRP-14 in the in vivo pathogenesis of gout.

Main Methods:

  • Quantification of MRP-8/MRP-14 in patient serum and synovial fluid using ELISA.
  • Immunohistochemical localization of MRPs in synovial tissue from gout patients.
  • In vitro analysis of MRP effects on IL-1β secretion using phagocytes, Western blotting, and PCR.
  • In vivo evaluation in a murine model of MSU crystal-induced peritonitis.

Main Results:

  • Elevated MRP-8/MRP-14 levels were observed in gout patients' synovium, tophi, and serum, correlating with disease activity.
  • MSU crystal-activated phagocytes released MRP-8/MRP-14, enhancing IL-1β secretion in a TLR-4-dependent manner.
  • Targeted deletion of MRP-14 in mice resulted in a moderately reduced inflammatory response to MSU crystals.

Conclusions:

  • MRP-8 and MRP-14 are significantly expressed in gout and enhance MSU crystal-induced IL-1β secretion both in vitro and in vivo.
  • These endogenous TLR-4 ligands, released by activated phagocytes, play a role in sustaining gout inflammation.
  • MRP-8 and MRP-14 represent potential therapeutic targets for managing gout.

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