Recent advances in crystal-induced acute inflammation.
PURPOSE OF REVIEW: The aim of this article is to highlight recent advances suggesting essential involvement of the innate immune system in crystal-induced acute inflammation. RECENT FINDINGS: 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. SUMMARY: These studies provided a new insight into the mechanisms underlying the initiation and the termination of monosodium urate monohydrate crystal-induced acute inflammation.[1]References
- Recent advances in crystal-induced acute inflammation. Akahoshi, T., Murakami, Y., Kitasato, H. Current opinion in rheumatology (2007) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
