Induction of triggering receptor expressed on myeloid cells 1 in murine resident peritoneal macrophages by monosodium urate monohydrate crystals

Wiley - Tập 54 Số 2 - Trang 455-462 - 2006
Yousuke Murakami1, Tohru Akahoshi2, Izumi Hayashi3, Hirahito Endo2, Shinichi Kawai4, Matsuhisa Inoue2, Hirobumi Kondo2, Hidero Kitasato5
1Kitasato Univ. School of Medicine, Kanagawa, Japan
2Graduate School of Medical Sciences, Kanagawa, Japan
3Nihon Pharmaceutical University, Saitama, Japan
4Toho University School of Medicine, Tokyo, Japan
5Kitasato University School of Allied Health Sciences and Graduate School of Medical Sciences, Kanagawa, Japan

Tóm tắt

AbstractObjectiveTriggering receptor expressed on myeloid cells 1 (TREM‐1) is a cell surface molecule that was recently identified on monocytes and neutrophils. TREM‐1 has been implicated in the early inflammatory responses induced by microbes, but its pathophysiologic role in nonmicrobial inflammation remains unknown. In the present study, we investigated the role of TREM‐1 in acute inflammation induced by monosodium urate monohydrate (MSU) crystals. Induction of TREM‐1 expression by MSU crystal–stimulated murine resident peritoneal macrophages and infiltrating leukocytes in a murine air‐pouch model of crystal‐induced acute inflammation was determined. The biologic role of TREM‐1 in crystal‐induced cytokine production by resident peritoneal macrophages was also investigated.MethodsTREM‐1 expression by resident peritoneal macrophages and infiltrating leukocytes in a murine air‐pouch model was determined by quantitative real‐time polymerase chain reaction, Western blot analysis, and flow cytometry. Cytokine production by resident peritoneal macrophages after incubation with MSU crystals in the presence or absence of an anti–TREM‐1 agonist antibody was determined by enzyme‐linked immunosorbent assay.ResultsTREM‐1 expression by resident peritoneal macrophages was significantly induced after stimulation with the crystals. Maximum expression of TREM‐1 transcripts and protein occurred at 1 and 4 hours after exposure to the crystals, respectively. Costimulation of resident peritoneal macrophages with MSU crystals and an anti–TREM‐1 agonist antibody synergistically increased the production of both interleukin‐1β and monocyte chemotactic protein 1 compared with stimulation with the crystals alone. MSU crystals also induced TREM‐1 expression in infiltrating leukocytes in a murine air‐pouch model of crystal‐induced acute inflammation.ConclusionThese findings suggest that rapid induction of TREM‐1 expression on resident peritoneal macrophages and neutrophils by MSU crystals may contribute to the development of acute gout through enhancement of inflammatory responses.

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Tài liệu tham khảo

10.1016/S0002-9343(97)89546-0

Terkeltaub RA, 2001, Arthritis and allied conditions, 2329

Di Giovine FS, 1987, Interleukin‐1 (IL‐1) as a mediator of crystal arthritis: stimulation of T cell and synovial fibroblast mitogenesis by urate crystal‐induced IL‐1, J Immunol, 138, 3213, 10.4049/jimmunol.138.10.3213

10.1172/JCI115142

Matsukawa A, 1998, Analysis of the cytokine network among tumor necrosis factor‐α, interleukin‐1β, interleukin‐8, and interleukin‐1 receptor antagonist in monosodium urate crystal‐induced rabbit arthritis, Lab Invest, 78, 559

Matsukawa A, 1998, Production and regulation of monocyte chemoattractant protein‐1 in lipopolysaccharide‐ or monosodium urate crystal‐induced arthritis in rabbits: roles of tumor necrosis factor‐α, interleukin‐1, and interleukin‐8, Lab Invest, 78, 973

10.1038/nri1106

10.4049/jimmunol.164.10.4991

10.1086/374754

10.4049/jimmunol.170.7.3812

10.1038/35074114

10.1084/jem.20040708

10.1016/S0002-9440(10)63915-6

10.4049/jimmunol.174.8.5016

10.1001/jama.1962.03050190031006

10.1074/jbc.M404368200

10.1002/1529-0131(199805)41:5<900::AID-ART18>3.0.CO;2-K

10.1002/art.10468

10.1002/art.11271

Coyne CP, 1993, Inhibition of lipopolysaccharide‐induced macrophage tumor necrosis factor‐α synthesis by polymyxin B sulfate, Am J Vet Res, 54, 305, 10.2460/ajvr.1993.54.02.305

10.1002/anr.1780321114

10.4049/jimmunol.173.12.7131

10.1074/jbc.M403823200

10.1073/pnas.94.5.1931

10.4049/jimmunol.154.3.1350

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Wiley

Tập 54 Số 2

455-462

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