Polypeptide growth factors augment interleukin 1-induced release of prostaglandin E2 by rheumatoid arthritis synovial cells in vitro

When stimulated with increasing amounts of interleukin 1β(IL, 1β) rheumatoid arthritis (RA), as compared with osteoarthritis (OA), synovial cells grown in RPMI plus fetal bovine serum (FBS), released significantly more prostaglandin E2 (PGE2) (p < 0.05; paired t test, two-tailed). PGE2 release by IL 1β-stimulated RA synovial cells grown for 14 days in serum-free RPMI was significantly less than that released by the same cells grown in medium plus 10% FBS (p < 0.03; two-tailed). Since these data suggest that growth factors present in FBS may augment the effects of IL 1β, experiments were conducted to study the influence of four polypeptide growth factors—transforming growth factor-β (TGF-β), platelet-derived growth factor (PDGF), epidermal growth factor (EGF), and basic fibroblast growth factor (bFGF), on IL 1β-induced release of PGE2 by cultured RA synovial cells. Both EGF and bFGF significantly enhanced IL 1β-induced release of PGE2 (p < 0.05; paired t test, one-tailed), while PDGF was synergistic with IL 1β, significantly increasing release of PGE2 by these cultured cells (p < 0.02; two-tailed). No such effect was seen when TGF-β was added to the culture medium. Taken together, these data lend support to the concept that within the synovial micro-environment small quantities of individual growth factors may potentiate the effects of IL 1β to amplify intra-articular inflammation.