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Mediators of Inflammation - Volume 9 2000, Issue 3-4, Pages 189-191



Department of Biology and Health Science, Faculty of Science, Technology andDesign, University of Luton, Park Square, Luton LU1 3JU, UK

Gastrointestinal Laboratory, The Rayne Institute, St Thomas′ Hospital, London SE1 7EH, UK



Copyright © 2000 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Basal, lipopolysaccharide LPS and silica-stimulated prostaglandin PG production were compared between peripheral blood mononuclear cells PBMNC from UC patients and healthy subjects HS. Basal and LPS-stimulated PBMNC PGI2, but not PGE2, production was greater in UC. LPS stimulated both PGE2 and PGI2 by PBMNC from HS and UC patients. Silica stimulated production of both PGs by cells from HS but only PGE2 by cells from UC patients. The differences in responses to silica and LPS may result from differences in activation of NFκB or, alternatively, prior sensitisation to one of these agents. That PBMNC PGE2 production is not increased in UC, as it is in Crohn’s disease, suggests that there are differences in PBMNC behaviour between these two diseases.





Autor: Neville A. Punchard, John Cason, Jonathan Mullins, Chaman Chander, and Richard P. H. Thompson

Fuente: https://www.hindawi.com/



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