alexa Sophisticate Mechanisms and Unsolved Problems in the Resolution of Acute Gouty Arthritis

Journal of Cytokine Biology
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Sophisticate Mechanisms and Unsolved Problems in the Resolution of Acute Gouty Arthritis

Song-Chou Hsieh1 and Chia-Li Yu2*

1Department of Internal Medicine, National Taiwan University Hospital, National Taiwan University College of Medicine, Taipei, Taiwan

2Institute of Molecular Medicine, National Taiwan University College of Medicine, Taipei, Taiwan

*Corresponding Author:
Chia-Li Yu
Institute of Molecular Medicine
National Taiwan University College of Medicine
#7 Chung-Shan South Road, Taipei 100, Taiwan
Tel: +886223957801
Fax: +886223957801
E-mail: [email protected]

Received Date: March 22, 2016; Accepted Date: June 03, 2016; Published Date: June 08, 2016

Citation: Hsieh SC, Yu CL (2016) Sophisticate Mechanisms and Unsolved Problems in the Resolution of Acute Gouty Arthritis. J Cytokine Biol 1:107. doi: 10.4172/jcb.1000107

Copyright: © 2016 Hsieh SC, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited



Only primates suffer from hyperuricemia and gout. Acute gouty attack with fulminate inflammation may recover within 7-10 days. The pathogenesis of monosodium urate monohydrate (MSU) crystal-induced acute gouty inflammation has been gradually elucidated. It is conceivable that MSU crystals possess both danger-associated pathological pattern (DAMP) and physical microcrystal properties that may activate innate immune cells IL-1 production and subsequent IL-6, IL-8 and TNF-α release from neighborhood cells. By contrast, the molecular basis of acute gouty inflammation resolution mostly remains unclear. Previous studiesdemonstrated that intracellular negative cytokine regulators CIS and SOCS-3 involved in the resolution of acute gouty inflammation in synergism with anti-inflammatory cytokine molecules (TGF-β1, IL-10 and soluble TNF-α receptors type 1 and 2). This commentary aims to dissect the potential mechanisms of induction and resolution of acute gouty attack. Besides, the unsolved problems in these issues are discussed.

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