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[痛风性关节炎的病理机制]

[Pathological mechanisms of gouty arthritis].

作者信息

Akahoshi Tohru

机构信息

Department of General Medicine, Kitasato University School of Medicine.

出版信息

Nihon Rinsho. 2008 Apr;66(4):705-10.

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.

摘要

痛风是一种由单水尿酸钠(MSU)晶体沉积引起的疾病。然而,急性痛风发作的确切机制尚不清楚。最近的研究为急性痛风的病理学提供了新证据。一些研究表明,MSU晶体可作为一种类似于外源性佐剂的“危险信号”,Toll样受体(TLR)介导的途径和/或MyD88依赖性白细胞介素-1受体途径参与急性痛风。已证实MSU晶体刺激可使吞噬细胞中髓样细胞表达的触发受体1(TREM-1)上调。此外,NALP 3炎性小体在痛风中的病理意义也已得到证实。这些发现为MSU晶体诱导急性炎症的起始机制提供了新的见解。

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