[Pathological mechanisms of gouty arthritis]

Nihon Rinsho. 2008 Apr;66(4):705-10.
[Article in Japanese]

Abstract

Gout is a disease caused by the deposition of monosodium urate monohydrate (MSU) crystals. Precise mechanisms underlying the initiation of acute gout, however, are not known. Recent investigations provided novel evidence in the pathology of acute gout. A number of studies indicated that MSU crystals can act as a "danger signal" which resembles exogenous adjuvants, and toll-like receptor(TLR)-mediated pathways and/or MyD88-dependent IL-1 receptor pathways are involved in acute gout. Up-regulation of the triggering receptor expressed on myeloid cells 1(TREM-1) in phagocytes by the stimulation with MSU crystals has been demonstrated. Furthermore, pathological significance of NALP 3 inflammasome in gout has been also demonstrated. These findings provide a new insight into the mechanisms underlying the initiation of MSU crystal-induced acute inflammation.

Publication types

  • Review

MeSH terms

  • Acute Disease
  • Arthritis, Gouty / etiology*
  • Carrier Proteins
  • Crystallization
  • Humans
  • Immunity, Innate / genetics
  • Interleukin-1beta / physiology
  • Lipopolysaccharide Receptors
  • Membrane Glycoproteins
  • Myeloid Differentiation Factor 88
  • NLR Family, Pyrin Domain-Containing 3 Protein
  • Receptors, Immunologic
  • Receptors, Interleukin-1
  • Toll-Like Receptors
  • Triggering Receptor Expressed on Myeloid Cells-1
  • Uric Acid / metabolism

Substances

  • Carrier Proteins
  • Interleukin-1beta
  • Lipopolysaccharide Receptors
  • MYD88 protein, human
  • Membrane Glycoproteins
  • Myeloid Differentiation Factor 88
  • NLR Family, Pyrin Domain-Containing 3 Protein
  • NLRP3 protein, human
  • Receptors, Immunologic
  • Receptors, Interleukin-1
  • TREM1 protein, human
  • Toll-Like Receptors
  • Triggering Receptor Expressed on Myeloid Cells-1
  • Uric Acid