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Reciprocal interaction between macrophage migration inhibitory factor and interleukin-8 in gout

1, 2, 3, 4, 5, 6

 

  1. Conversant Research Consortium in Immunologic disease, Seoul St. Mary's Hospital, The Rheumatism Research Center, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul, Korea.
  2. Conversant Research Consortium in Immunologic disease, Seoul St. Mary's Hospital, The Rheumatism Research Center, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul, Korea.
  3. Division of Rheumatology, Department of Internal Medicine, Konkuk University School of Medicine, Konkuk University Medical Center, Seoul, Korea.
  4. Division of Rheumatology, Department of Internal Medicine, The Soonchunhyang University Seoul Hospital, Seoul, Korea.
  5. Division of Rheumatology, Department of Internal Medicine, Konkuk University School of Medicine, Konkuk University Medical Center, Seoul, Korea.
  6. Division of Rheumatology, Department of Internal Medicine, Konkuk University School of Medicine, Konkuk University Medical Center, Seoul, Korea. kimhaerim@kuh.ac.kr

CER11150
2019 Vol.37, N°2
PI 0270, PF 0278
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PMID: 30148447 [PubMed]

Received: 01/02/2018
Accepted : 29/05/2018
In Press: 19/07/2018
Published: 19/03/2019

Abstract

OBJECTIVES:
Macrophage migration inhibitory factor (MIF) is a proinflammatory, chemotactic, and tissue destructive cytokine. This study determined monosodium urate crystal-induced MIF production and its interaction with interleukin (IL)-8 in gout.
METHODS:
Peripheral blood (PB), synovial fluid (SF), and clinical data were obtained from 98 patients with gout. SF and serum concentrations of MIF and IL-8 were measured using ELISA. SF monocytes and neutrophils were cultured with monosodium urate (MSU) crystals and the cytokine production was determined. The signalling pathways involved were determined using signal inhibitors. The interaction between MIF and IL-8 was investigated.
RESULTS:
SF MIF was higher in acute gout and that in serum was higher in patients with intercritical gout compared with controls. SF MIF was positively correlated with SF leukocyte and neutrophil counts and IL-8. The expression of MIF was similar in SF neutrophils and monocytes, while IL-8 was higher in monocytes. MSU crystals induced MIF production in monocytes and IL-8 production in neutrophils. This effect was decreased by inhibiting Fc-gamma receptor 1 and toll-like receptor 4. IL-8 increased MIF production in monocytes while MIF increased interleukin-8 production in neutrophils.
CONCLUSIONS:
MIF and IL-8 are highly produced in acute gout. MSU crystals induced MIF production in monocytes and IL-8 production in neutrophils with a reciprocal interaction between the two cytokines.

Rheumatology Article