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Eicosanoid production by human monocytes: does COX-2 contribute to a self-limiting inflammatory response?

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dc.contributor.authorJames, M.
dc.contributor.authorPenglis, P.
dc.contributor.authorCaughey, G.
dc.contributor.authorDemasi, M.
dc.contributor.authorCleland, L.
dc.date.issued2001
dc.description.abstractThe eicosanoids, prostaglandin E2 (PGE2) and thromboxane A2 (TXA2), are involved in inflammatory events. TXA2 has potentially pro-inflammatory actions and PGE2 has actions which can be considered both pro- and antiinflammatory. Therefore, it is potentially significant that production of TXA2 and PGE2 by stimulated monocytes have very different time courses. TXA2 synthesis is immediate and dependent on cyclooxygenase Type 1 (COX-1) activity whereas PGE2 synthesis is delayed and dependent on COX-2 activity. These apparent COX-isotype dependencies of TXA2 and PGE2 synthesis can be explained by differences in the affinities of TXA synthase and PGE synthase for the common substrate, PGH2. The findings have implications for the use of NSAIDs and selective COX-2 inhibitors whose actions can increase the monocyte TXA2/PGE2 ratio.
dc.description.statementofresponsibilityJames, M. J. ; Penglis, P. S. ; Caughey, G. E. ; Demasi, M. ; Cleland, L. G.
dc.identifier.citationInflammation Research, 2001; 50(5):249-253
dc.identifier.doi10.1007/s000110050750
dc.identifier.issn1023-3830
dc.identifier.issn1420-908X
dc.identifier.orcidJames, M. [0000-0002-4918-2998]
dc.identifier.orcidCaughey, G. [0000-0003-1192-4121]
dc.identifier.urihttp://hdl.handle.net/2440/9511
dc.language.isoen
dc.publisherBirkhauser Verlag Ag
dc.source.urihttps://doi.org/10.1007/s000110050750
dc.subjectMonocytes
dc.subjectHumans
dc.subjectInflammation
dc.subjectIsoenzymes
dc.subjectEicosanoids
dc.subjectMembrane Proteins
dc.subjectProstaglandin-Endoperoxide Synthases
dc.subjectCyclooxygenase 2
dc.titleEicosanoid production by human monocytes: does COX-2 contribute to a self-limiting inflammatory response?
dc.typeJournal article
pubs.publication-statusPublished

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