       Document 0102
 DOCN  M9550102
 TI    Prostaglandin-E2 is a potent inhibitor of human interleukin 12
       production.
 DT    9505
 AU    van der Pouw Kraan TC; Boeije LC; Smeenk RJ; Wijdenes J; Aarden LA;
       Department of Autoimmune Diseases, Central Laboratory of the;
       Netherlands Red Cross Blood Transfusion Service, Amsterdam.
 SO    J Exp Med. 1995 Feb 1;181(2):775-9. Unique Identifier : AIDSLINE
       MED/95138710
 AB    During human immunodeficiency virus infection and allergic diseases,
       characterized by a dominant T helper (Th) 2 response, overproduction of
       prostaglandin E2 (PGE2) is observed. In this paper we studied the effect
       of PGE2 on interleukin (IL)-12 synthesis, because this cytokine has been
       described to be essential in induction of Th1 responses. IL-12 synthesis
       was induced in monocytes that were stimulated with Neisseria
       meningitidis-derived lipopolysaccharide in whole blood cultures. PGE2
       almost completely inhibited lipopolysaccharide induced IL-12 production,
       whereas IL-6 production was only partially inhibited by PGE2. In
       contrast, the production of IL-10 was approximately twofold enhanced at
       these conditions. The effects of PGE2 were due to its cAMP-inducing
       capacity, since they could be mimicked by other cAMP inducers.
       Recombinant human IL-10 also inhibited IL-12 and IL-6 production.
       However, the inhibitory effect of PGE2 on IL-12 production was
       independent of IL-10 since neutralizing anti-IL-10 antibodies were
       unable to reverse this inhibition. These results suggest that the
       capacity of an antigen to induce PGE2 synthesis may play a crucial role
       in the development of either a Th1 or Th2 response.
 DE    Cyclic AMP/METABOLISM/PHARMACOLOGY  Dinoprostone/*PHARMACOLOGY  Human
       In Vitro  Interleukin-10/BIOSYNTHESIS  Interleukin-12/*ANTAGONISTS &
       INHIB/BIOSYNTHESIS  Interleukin-6/BIOSYNTHESIS
       Lipopolysaccharides/PHARMACOLOGY  Support, Non-U.S. Gov't  JOURNAL
       ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).

