Macrophage inflammatory protein 1 alpha expression by synovial fluid neutrophils in rheumatoid arthritis

doi:10.1136/ard.58.5.297

Annals of the Rheumatic Diseases 1999;58:297-302; doi:10.1136/ard.58.5.297

Ann Rheum Dis 1999;58:297-302 ( May )

Extended reports

Macrophage inflammatory protein 1 alpha expression by synovial fluid neutrophils in rheumatoid arthritis Yoshimi Hatano,^a Tsuyoshi Kasama,^a Hideaki Iwabuchi,^a Ryosuke Hanaoka,^a Hiroko T Takeuchi,^a Lu Jing,^a Yoshiaki Mori,^b Kazuo Kobayashi,^c Masao Negishi,^a Hirotsugu Ide,^a Mitsuru Adachi^a

^a The First Department of Internal Medicine, Showa University School of Medicine, Tokyo, Japan, ^b Department of Physical Medicine and Rehabilitation, Showa University School of Medicine, Tokyo, Japan, ^c Department of Host Defenses, National Institute of Infectious Diseases, Tokyo, Japan

Correspondence to: Dr T Kasama, The First Department of Internal Medicine Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8666, Japan.

Accepted for publication 18 January 1999

OBJECTIVE $---$ To determine the contribution made by synovial fluid (SF) neutrophils to the augmented expression of macrophage inflammatoryprotein 1 $alpha$ (MIP-1 $alpha$ ) in rheumatoid arthritis(RA).
METHODS $---$ Neutrophils were isolated from samples of SF from RA patients and peripheral blood (PB) samples from RA patients and healthycontrols. Cell associated MIP-1 $alpha$ was visualised immunohistochemically,and cell associated MIP-1 $alpha$ as well as MIP-1 $alpha$ secreted into theSF was assayed by ELISA. Steady state expression of MIP-1 $alpha$ mRNAwas assessed by reverse transcription polymerase chain reaction(RT-PCR).
RESULTS $---$ Freshly isolated SF neutrophils contained significantly higher concentrations of both MIP-1 $alpha$ protein and its transcript thanPB neutrophils from either RA patients or healthy controls; incubationin the absence or presence of tumour necrosis factor $alpha$ for 24hours resulted in a significant increase in MIP-1 $alpha$ secretion byRA SF neutrophils compared with neutrophils obtained from eithernormal PB or RA PB; and expression of MIP-1 $alpha$ by SF neutrophilswas well correlated with both RA disease activity and SF mononuclearcell (MNC)counts.
CONCLUSION $---$ Expression and secretion of MIP-1 $alpha$ by SF neutrophils may be indicative of local and systemic inflammation in RA. Moreover,this C-C chemokine may contribute to the recruitment of MNCs fromthe bloodstream into synovial joints andtissues.

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