Monosodium urate crystal-induced triggering receptor expressed on myeloid cells 1 is associated with acute gouty inflammation

• Published in: Rheumatology (Oxford, England) England), 2016-01, Vol.55 (1), p.156-161
• Main Authors: Lee, Jennifer, Lee, Seon-Young, Lee, Jaeseon, Lee, Juhyun, Baek, Seungye, Lee, Dong-Gun, Kim, Eun-Kyung, Lee, Sung Hak, Cho, Mi-La, Kwok, Seung-Ki, Ju, Ji Hyeon, Park, Sung-Hwan
• Format: Article
• Language: English
• Subjects: Acute Disease; Enzyme-Linked Immunosorbent Assay; Flow Cytometry; Gene Expression Regulation; Gout - genetics; Gout - metabolism; Gout - pathology; Humans; Immunohistochemistry; Membrane Glycoproteins - biosynthesis; Membrane Glycoproteins - genetics; Myeloid Cells - metabolism; Myeloid Cells - pathology; Real-Time Polymerase Chain Reaction; Receptors, Immunologic - biosynthesis; Receptors, Immunologic - genetics; Retrospective Studies; RNA - genetics; Triggering Receptor Expressed on Myeloid Cells-1; Uric Acid - metabolism
• ISSN: 1462-0324; 1462-0332
• DOI: 10.1093/rheumatology/kev316

Triggering receptor expressed on myeloid cells 1 (TREM-1), which amplifies the inflammation elicited by the Toll-like receptor pathway, was originally implicated in sepsis and bacterial infection. However, it has been suggested that TREM-1 may also play an important role in non-infectious inflammation. The present study was conducted to investigate whether TREM-1 is involved in human acute gouty inflammation. A total of 37 gout patients were recruited between March 2011 and January 2014 from Seoul St Mary's Hospital. The expression of TREM-1 on mononuclear cells was assessed using FACS analysis, immunostaining and real-time RT-PCR. To block the TREM-1 signal, soluble TREM-1 (sTREM-1) or the synthetic blocking peptide LP17 was used. The concentration of sTREM-1 was assessed by ELISA. FACS analysis and real-time RT-PCR demonstrated that TREM-1 expression was higher in the SF mononuclear cells of acute gouty arthritis patients than in peripheral blood mononuclear cells (PBMCs). Immunohistochemical staining of tophi tissues revealed TREM-1 expression, with confocal microscopy demonstrating TREM-1 expression on tophi tissue macrophages. We also demonstrated that MSU treatment induced TREM-1 expression on the PBMCs of acute gout patients in vitro. Although blockade of TREM-1 did not directly suppress MSU-induced IL-1β production of PBMCs in vitro, the concentration of soluble TREM-1 was higher in the SF of gout vs OA patients and was positively correlated with serum CRP. TREM-1 is induced by MSU and is associated with the inflammation of human acute gouty arthritis.