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Gout and Hyperuricemia March 2017
Gout and Hyperuricemia. 2017; 4(1): 21-26
DOI: 10.3966/GH1703040104
Abstract  |  Full Text (HTML)  |  Full Text (PDF)
T cell immunoglobulin and mucin domain molecule 4 is dispensable in monosodium urate-induced gouty inflammation in mice
Qi-Bin Yang1,3,4, Quan-Bo Zhang2,3,4, Yong-Long He1, Yu-Feng Qing1, Li Zhou3,4,5,6, Jing-Guo Zhou7,*, Qing-Sheng Mi3,4,5,6,*
1Department of Rheumatology and Immunology, Affiliated Hospital, North Sichuan Medical College, China. 2Department of Geriatrics, Affliated Hospital, North Sichuan Medical College, China. 3Henry Ford Immunology Program, Henry Ford Health System, Detroit, MI 48202. 4Department of Dermatology, Henry Ford Health System, Detroit, MI 48202. 5Department of Internal Medicine, Henry Ford Health System, Detroit, MI 48202. 6Department of Immunology and Microbiology, Wayne State University School of Medicine, Detroit, MI 48202. 7Department of Rheumatology and Immunology, Affiliated Hospital, Chengdu Medical College, China.

*Corresponding authors:
Dr. Jing-Guo Zhou
Department of Rheumatology and Immunology, Affiliated Hospital, Chengdu Medical College, China.
E-mail: jgzhou@cmc.edu.cn
Tel: 8613990880518

Dr. Qing-Sheng Mi
Henry Ford Immunology Program, Departments of Dermatology and Internal Medicine, Henry Ford Health System, 1 Ford Place, Detroit, MI, United States.
E-mail: qmi1@hfhs.org
Tel: +1-313-876-1017
Fax: 313-876-1016


Submitted on Apr. 5, 2017; accepted on Apr. 26, 2017.
©2017, Gout and Hyperuricemia. Published by Dong Fong Health Co. LTD in Taiwan. All right reserved.
Abstract
Objective:Gouty arthritis is a sharp inflammatory arthritis induced by monosodium urate (MSU) crystals. Previous studies indicate that the T cell immunoglobulin and mucin domain molecule 4 (TIM-4) is an adhesive molecule which binds to phosphatidylserine (PS) to mediate phagocytosis of apoptotic cells by macrophages, which also regulate T cell activation and increase proinflammatory cytokine expression. This study aims to investigate whether TIM-4 is involved in MSU-induced gouty inflammation.
Methods:MSU suspensions were injected into ankle joints or foot pads of TIM-4 knock-out (KO) and wild type (WT) mice to induce acute gout. Ankle swelling or paw edema were measured at different time points with digital caliper. MSU suspensions were injected into peritoneal cavity or air pouch. Peritoneal cavity or air pouch exudate cells were then harvested after 3 or 6 hours and the infiltrated macrophages and neutrophils were counted by Fluorescence-Activated Cell Sorting (FACS).
Results:In the ankle joints model of MSU-induced gouty arthritis, ankle joint swelling index in TIM-4 KO mice was not significantly different compared with WT mice. Consistent with the ankle joints model, the paw swelling index also had no difference in TIM-4 KO mice compared with WT controls. Additionally, there were no dramatic changes in total number of peritoneal cavity or air pouch exudate cells, neutrophils influxes and infiltrated macrophages between KO and WT mice.
Conclusion:TIM-4 may not play a crucial role in the development of MSU-induced gouty inflammation.

Key words:TIM-4; Gout; Inflammation