Background Chemokines play a key role in modulating leukocyte functions at sites of inflammation. In rheumatoid arthritis (RA) an enhancement of the chemokine macrophage inflammatory protein-1alpha (MIP-1a) was observed and may be indicative for inflammatory processes.1 In addition to its proinflammatory activities several lines of evidence indicate that MIP-1a modulates the proliferation of hematopoietic progenitor cells.2
Anaemia is a common feature of active rheumatoid arthritis. Very little information on the significance of MIP-1a on the pathogenesis of anaemia in RA is available.
Objectives Basing on theoretical, haematological and immunological data, the chemokine MIP-1a was to be determined about its importance in RA concerning the activity of inflammation and the development of anaemia.
Methods 84 patients (18 male, 66 female) with rheumatoid arthritis (ACR criteria) were included to detect inflammatory processes and anaemia. White and red blood cell count, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), serum iron and the rheumatoid factor were assessed by routine laboratory methods. MIP-1a, serum amyloid A (SAA) and transferrin receptor (TfR) were measured by solid phase enzyme immunoassay; erythropoietin (EPO) and neopterin by radioimmunoassay techniques.
Results High MIP-1a levels were accompanied by increased parameters of inflammation (SAA, CRP, ESR). Patients with RA and anaemia showed significantly higher MIP-1a levels than those without anaemia (p < 0.03). However, high MIP-1a levels together with decreased serum iron were not associated with increased EPO levels. It might be of importance that patients with high MIP-1a levels in parallel with anaemia and activation of inflammation had a twofold frequency of disability pension compared to RA patients without anaemia.
Conclusion The enhanced expression of MIP-1a in RA is indicative of the inflammatory activation. Moreover besides the regulation of inflammatory processes this chemokine may influence the pathogenesis of anaemia in RA.
Koch AE, Kunkel SL, Harlow LA, et al. Macrophage inflammatory protein-1 alpha. A novel chemotactic cytokine for macrophages in rheumatoid arthritis. J Clin Invest. 1994;93: 921–8
Su SB, Mukaida N, Wang JB, Zhang Y, Takami A, Nakao S, Matsushima K. Inhibition of immature erythroid progenitor cell proliferation by macrophage inflammatory protein-1a by interacting mainly with a C-C chemokine receptor, CCR1. Blood 1997;90(2):605–11
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