Control of collagen synthesis in human chondrocyte cultures by immune interferon and interleukin-1.
Academic Article
Overview
abstract
A cell culture model has been established employing normal human articular or costal chondrocytes in monolayer culture as target cells for the effects of intercellular mediators on chondrocyte function, particularly collagen synthesis. Recombinant Interleukin-1 (IL-1) which stimulates the synthesis of prostaglandin E2 (PGE2), collagenase, and plasminogen activator also stimulates the synthesis of collagen and increases steady-state levels of mRNA in cultured chondrocytes, synovial cells and foreskin fibroblasts if the synthesis of PGE2, which inhibits collagen synthesis, is inhibited by indomethacin. Recombinant immune interferon (IFN-gamma), which does not affect collagenase of PGE2 production, suppresses type II as well as types I and III collagen synthesis and associated mRNA levels. IL-1 and IFN-gamma could therefore have opposite roles in modulating cartilage matrix turnover in joint disease by affecting repair as well as degradation.