The Participation of IL-8 in the Synovial Lesions at an Early Stage of Rheumatoid Arthritis.

Abstract

Synovial tissues from Rheumatoid Arthritis (RA) were divided into three groups based on their histopathological findings and compared for their expression of IL-8 and monocyte chemotactic and activating factor (MCAF) by using immunohistochemistry and in situ hybridization. The levels of IL-8 as well as those of MCAF were markedly higher in the synovial fluid from RA joints. Synovial lining cells (SLC) and macrophages had an ability to produce IL-8 at an early phase of the disease. The presence of MCAF was restricted in macrophages at this stage. On the other hand, the production of IL-8 as well as MCAF were prominent in most components of the joints such as SLC, migrated monocytes, sublining fibroblastoid cells, endothelial cells or migrated neutrophils at an active phase. The expression of IL-8 or MCAF was low in fibrotic synovitis of RA. These data indicate that IL-8 generated from SLC and macrophages may participate to the inflammatory process in the early synovitis of RA.

Decreased ex vivo production of TNF-α and IL-8 by peripheral blood cells of patients with rheumatoid arthritis after infliximab therapy

“…This study shows that the ex vivo release of IL-8 from peripheral blood cells of patients with RA was decreased upon mitogen activation after infliximab therapy. Since the regulated movement of immune cells is highly dependent on the chemokine network [22], the decreased production of IL-8 from peripheral blood cells suggests a diminished recruitment of neutrophils from blood circulation to the sites of inflammation [21]. This is in concordance with our previous published findings that a significant and rapid reduction in inflammation of the synovial joints was observed after the addition of infliximab to MTX therapy in patients with active RA [15].…”

“…IL-8/CXCL8, also called neutrophil-activating peptide-1, is a CXC chemokine. It is a potent neutrophil chemoattractant and its concentration has been shown to be significantly higher in clinically inflamed joints in RA [21]. This study shows that the ex vivo release of IL-8 from peripheral blood cells of patients with RA was decreased upon mitogen activation after infliximab therapy.…”

Serum chemokines in patients with rheumatoid arthritis treated with etanercept

“…In addition, chemokines promote synthesis of proinflammatory cytokines like IL-1, IL-6, TNF-α or matrix metalloproteinases engaged in the joint destruction in RA [3,7]. Abundant presence of such chemokines like IL-8, RANTES (regulated upon activation, normal T cell expressed and secreted) or MCP-1 in rheumatoid synovium even in early stage of the disease, support the role of chemokines in RA [8,9,10].…”

Insoluble and soluble immune complexes activate neutrophils by distinct activation mechanisms: changes in functional responses induced by priming with cytokines

“…14 Rheumatoid synovial fluid is also a rich source of cytokines (for example, GM-CSF, interleukin 1, interferon γ) that can affect the function of infiltrating neutrophils. [15][16][17][18] One notable effect of cytokines is their ability to "prime" neutrophil functions so that their responsiveness to stimulation is greatly enhanced. 2 19 20 The aims of this study were several-fold.…”

“…[15][16][17][18] One notable effect of cytokines is their ability to "prime" neutrophil functions so that their responsiveness to stimulation is greatly enhanced. 2 19 20 The aims of this study were several-fold.…”