| Literature DB >> 6321595 |
D Boraschi, S Censini, M Bartalini, G Scapigliati, G Barbarulli, E Vicenzi, M B Donati, A Tagliabue.
Abstract
Mouse resident peritoneal M phi produced considerable amounts of PGE when triggered in vitro with soluble or particulate stimuli. Preexposure of M phi to IFN-beta dramatically decreased PGE production. This effect depended on the dose of IFN-beta used and was abolished by anti-IFN-beta globulin. In addition to PGE, other AA metabolites of the cyclooxygenase pathway, namely TXB2 and 6-keto PGF1 alpha, were decreased in IFN-beta-treated M phi. However, IFN-beta did not have any effect on cyclooxygenase activity of M phi, indicating that an earlier step of PG biosynthesis was likely to be the target of its inhibitory action. Indeed, the release of radioactive compounds from M phi prelabeled with [14C]AA was strongly impaired by IFN-beta, suggesting that IFN-beta would decrease PG production in M phi by blocking phospholipase activation. The possibility that the IFN-beta effect on phospholipase could be mediated through the increase of the intracellular levels of cAMP is suggested.Entities:
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Year: 1984 PMID： 6321595
Source DB: PubMed Journal: J Immunol ISSN： 0022-1767 Impact factor: 5.422