[Interleukin 1, prostaglandin E2 and articular inflammation].
IL1 can be considered as a factor able to act both on the catabolism of the cartilagenous matrix and on its biosynthesis. A major objective of research into articular inflammation is therefore an understanding of the mechanisms which not only regulate the production of IL1 but also its effects on cells. In fact, prostaglandin E2 is involved in most of the mechanisms and its secretion is itself stimulated by IL1. This mediator therefore has a very important regulatory role in the network of interactions affecting the cells of the immune system and the connective cells. The aim of this work is to review present knowledge in this field and to demonstrate the influence of non-steroidal anti-inflammatory agents (NSAIAs) on certain interactions regulated by PGE2. Thus, in vitro experiments have shown that naproxen reduces the PGE2-dependent inhibitory effect exerted by IL1 on the biosynthesis of collagen and proteoglycans and suggest that this NSAIA may be of use in degenerative osteoarticular disease.
Pujol
J P
JP
Laboratoire de Biochimie du Tissu Conjonctif, CHU Côte de Nacre, Caen.
D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology; D001168:Arthritis / Q000276:immunology / Q000503:physiopathology*; D015232:Dinoprostone / Q000502:physiology*; D006801:Humans; D007375:Interleukin-1 / Q000502:physiology*; D009288:Naproxen / Q000494:pharmacology
D000894:Anti-Inflammatory Agents, Non-Steroidal; D007375:Interleukin-1; D009288:Naproxen; D015232:Dinoprostone
Interleukine 1, prostaglandine E2 et inflammation articulaire.