title: Recent advances in crystal-induced acute inflammation.
abstract: OBJECTIVE
  The aim of this article is to highlight recent advances suggesting essential involvement of the innate immune system in crystal-induced acute inflammation.
  
  
  RESULTS
  Gout is a disease caused by the deposition of monosodium urate monohydrate crystals. Precise mechanisms underlying the initiation of monosodium urate monohydrate crystal-induced acute inflammation, however, are not known. Recent investigations provided novel evidence in the pathology of acute gout. Immunological study indicated that monosodium urate monohydrate crystals can act as a 'danger signal' that resembles exogenous adjuvants. Two laboratories have documented interesting findings that Toll-like receptor-mediated pathways or MyD88-dependent pathways are involved in monosodium urate monohydrate crystal-induced acute inflammation. Upregulation of the triggering receptor expressed on myeloid cells 1 (TREM-1) in phagocytes by the stimulation with monosodium urate monohydrate crystals has been demonstrated. Furthermore, pathological significance of NALP 3 inflammasome in gout has been shown. These findings provide a new concept that the innate immune system may play a crucial role on the triggering of crystal-induced acute inflammation. Spontaneous resolution is a characteristic feature of acute gout. Involvement of nuclear hormone receptors, peroxisome proliferator-activated receptor gamma and liver X receptor alpha, during the termination of acute gout has been also shown.
  
  
  CONCLUSIONS
  These studies provided a new insight into the mechanisms underlying the initiation and the termination of monosodium urate monohydrate crystal-induced acute inflammation.
authors.affiliation: Department of General Medicine, Kitasato University School of Medicine, Kitasato, Sagamihara, Kanagawa, Japan. akahoshi@med.kitasato-u.ac.jp
authors.forename: Tohru
authors.initials: T
authors.lastname: Akahoshi
authors.forename: Yousuke
authors.initials: Y
authors.lastname: Murakami
authors.forename: Hidero
authors.initials: H
authors.lastname: Kitasato
mesh_terms: D000208:Acute Disease; D002352:Carrier Proteins / Q000276:immunology; D006073:Gout / Q000139:chemically induced / Q000276:immunology*; D006801:Humans; D007113:Immunity, Innate; D007249:Inflammation / Q000139:chemically induced*; D053583:Interleukin-1beta / Q000276:immunology; D008562:Membrane Glycoproteins / Q000276:immunology; D000071199:NLR Family, Pyrin Domain-Containing 3 Protein; D011971:Receptors, Immunologic / Q000276:immunology; D051193:Toll-Like Receptors / Q000276:immunology; D000073871:Triggering Receptor Expressed on Myeloid Cells-1; D014527:Uric Acid / Q000276:immunology*
chemical_list: D002352:Carrier Proteins; D053583:Interleukin-1beta; D008562:Membrane Glycoproteins; D000071199:NLR Family, Pyrin Domain-Containing 3 Protein; C453881:NLRP3 protein, human; D011971:Receptors, Immunologic; C408842:TREM1 protein, human; D051193:Toll-Like Receptors; D000073871:Triggering Receptor Expressed on Myeloid Cells-1; D014527:Uric Acid