Stimulation of rheumatoid synovial cell collagenase and prostaglandin production by partially purified lymphocyte-activating factor (interleukin 1).

Abstract

Human macrophages produce in culture a factor termed mononuclear cell factor (MCF) that increases the production of collagenase and prostaglandins by isolated adherent rheumatoid synovial cells. A factor with similar biologic activity is also produced by the murine macrophage cell line P388D1. By using a sequential purification scheme involving ammonium sulfate fractionation; chromatography on DEAE-cellulose, Sephacryl S-200, and phenyl-Sepharose; and discontinuous polyacrylamide gel electrophoresis, the P388D1 cell-derived, synovial cell-stimulating factor was -copurified with the lymphocyte-activating factor [LAF; interleukin 1 (IL 1)]. The specific activity of the partially purified LAF (IL 1) was approximately 15,000-fold higher than that of the LAF (IL 1) in the original P388D1 cell culture supernatant. On the basis of (i) the copurification of the P388D1 cell-derived LAF (IL 1) and synovial cell-stimulating factors; (ii) the similarity in cell of origin, molecular weight, and phenylglyoxal sensitivity of human MCF and murine LAF (IL 1); and (iii)

Pre-treatment with IL-1β enhances the efficacy of MSC transplantation in DSS-induced colitis

“…20,30 C57BL/6 mice were randomly divided into the following five groups (n510 mice/group): (i) control group; (ii) DSS treatment; (iii) DSS with MSC treatment; (iv) DSS with IL-1b-primed MSC treatment; (v) DSS with IL-1R1 siRNA-transfected MSC treatment (Table 2). At day 1, mouse tails were intravenously injected with 2310 6 MSCs (MSCs, IL-1b-primed or IL-1R1 siRNA-transfected MSCs) diluted in 200 ml PBS or a vehicle control (PBS alone).…”

“…18 IL-1b induces the production of cyclooxygenase-2 (COX-2), which promotes the expression of prostaglandin E2 (PGE2). 19,20 PGE2, in turn, has been reported to inhibit mucosal inflammation during DSS-induced colitis in mice and rats. 21,22 Similarly, pre-treatment with a low dose of IL-1b has also been shown to suppress colonic inflammation in rabbits via the production of PGE2.…”

Isolation of an interleukin‐1‐like factor from human joint effusions

“…tical to IL-1 markedly augments the secretion of prostaglandins and neutral proteases from synovial cells and chrondrocytes (2)(3)(4)(5). Although it remains to be resolved whether these various biologic activities are due to a single molecule or to a heterogeneous family of molecules, IL-1-like molecules clearly could be implicated in the pathogenesis of joint destruction.…”

Modulation of cartilage destruction by select nonsteroidal antiinflammatory drugs

“…IL-1 may have potential deleterious effects that contribute to cartilage and bone destruction beyond its property of inducing the synthesis and release of matrix-degrading proteinases from chondrocytes. It is able to stimulate chondrocyte release of prostaglandins and plasminogen activator (23,37), suppress chondrocyte glycosaminoglycan synthesis (38), induce the release of prostaglandins, plasminogen activator, and matrix-degrading proteinases from dendritic synoviocytes (39), induce bone resorption (40,41), and suppress bone collagen and osteocalcin synthesis (42). Therefore, pharmacologic intervention to modulate the synthesis and/or activity of IL-1 would appear to be highly desirable.…”