Jennifer Lee1, Seon-Young Lee2, Jaeseon Lee2, Juhyun Lee2, Seungye Baek1, Dong-Gun Lee1, Eun-Kyung Kim2, Sung Hak Lee3, Mi-La Cho2, Seung-Ki Kwok4, Ji Hyeon Ju1, Sung-Hwan Park5. 1. Division of Rheumatology, Department of Internal Medicine, School of Medicine, Catholic University of Korea, Seoul St Mary's Hospital. 2. Rheumatism Research Center, Catholic Research Institute of Medical Science, Catholic University of Korea and. 3. Department of Hospital Pathology, School of Medicine, Catholic University of Korea, Seoul St Mary's Hospital, Seoul, Republic of Korea. 4. Division of Rheumatology, Department of Internal Medicine, School of Medicine, Catholic University of Korea, Seoul St Mary's Hospital, Rheumatism Research Center, Catholic Research Institute of Medical Science, Catholic University of Korea and. 5. Division of Rheumatology, Department of Internal Medicine, School of Medicine, Catholic University of Korea, Seoul St Mary's Hospital, Rheumatism Research Center, Catholic Research Institute of Medical Science, Catholic University of Korea and rapark@catholic.ac.kr.
Abstract
OBJECTIVE: 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. METHODS: 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. RESULTS: 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. CONCLUSION: TREM-1 is induced by MSU and is associated with the inflammation of human acute gouty arthritis.
OBJECTIVE: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 humanacute gouty inflammation. METHODS: A total of 37 goutpatients 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. RESULTS: FACS analysis and real-time RT-PCR demonstrated that TREM-1 expression was higher in the SF mononuclear cells of acute gouty arthritispatients 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 goutpatients 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. CONCLUSION:TREM-1 is induced by MSU and is associated with the inflammation of human acute gouty arthritis.