Stimulation of prostaglandin E production in cultured human fibroblasts by poly(I) · poly(C) and human interferon

• DOI: 10.1038/267457a0
• Publication Date: 2005-08-03T06:12:03Z
• Authors: M. YARON; I. YARON; D. GURARI-ROTMAN; M. REVEL; H. R. LINDNER; U. ZOR
• Keywords: Prostaglandin E1; Foreskin

PROSTAGLANDINS (PGs) have emerged as one of the principal mediators of the inflammatory process1–3. Elevation of tissue concentration of PGs was noted following inflammation3,4, or treatment with various hormones5,6, cyclic nucleotides (ref. 7 and U.Z., B. Strulovici and H.R.L., in preparation), serum8, drugs8,9 and antigen10. The beneficial effects of anti-inflammatory drugs have been correlated with their ability to suppress PG production either by curtailing precursor availability (glucocorticosteroids11,12) or by inhibiting PG synthetase activity (non-steroidal drugs1). Viral infections are associated with interferon production13 and with inflammation14. Little is known about the possible involvement of interferon in the inflammatory reaction, though it has been suggested that interferon may have anti-inflammatory properties15. It has been shown that an interferon inducer, double-stranded polyinosinate·polycytidylate [poly(I)·poly(C)], as well as human interferon, stimulate hyaluronic acid production by human synovial fibroblasts in culture16. Overproduction of hyaluronic acid is known to be associated with the inflammatory process16; the effect is prevented by cortisol or indomethacin16. We report here the stimulation by poly(I)·poly(C) and by human interferon of prostaglandin E (PGE) production by human synovial and foreskin fibroblasts in culture. Cortisol inhibited this effect.