Picture water droplets

Developing mathematical theories of the physical world: Open Access research on fluid dynamics from Strathclyde

Strathprints makes available Open Access scholarly outputs by Strathclyde's Department of Mathematics & Statistics, where continuum mechanics and industrial mathematics is a specialism. Such research seeks to understand fluid dynamics, among many other related areas such as liquid crystals and droplet evaporation.

The Department of Mathematics & Statistics also demonstrates expertise in population modelling & epidemiology, stochastic analysis, applied analysis and scientific computing. Access world leading mathematical and statistical Open Access research!

Explore all Strathclyde Open Access research...

Cytokines and cytokine inducers stimulate prostaglandin E2 entry into the brain

Davidson, J. and Abul, H.T. and Milton, A.S. and Rotondo, D. (2001) Cytokines and cytokine inducers stimulate prostaglandin E2 entry into the brain. Pflugers Archiv - European Journal of Physiology, 442 (4). pp. 526-533. ISSN 0031-6768

Full text not available in this repository. Request a copy from the Strathclyde author


Cytokine inducers and cytokines increase the circulating level of prostaglandin E2 (PGE2) during the acute-phase immune response. This occurs simultaneously with the onset of fever, indicating that brain levels of PGE2 also increase. This raises the possibility that PGE2 produced in the peripheral circulation, not necessarily at distant sites from the brain, may penetrate the brain and be present in the cerebrospinal fluid (CSF). Blood and CSF levels of PGE2 in rabbits were measured by radioimmunoassay during fever stimulated in response to lipopolysaccharide (LPS), polyinosinic:polycytidylic acid (poly I:C) and interleukin-1 (IL-1) given i.v. The effect of the prostaglandin synthesis inhibitor ketoprofen on these parameters was also studied. In addition, the level of radioactivity in the CSF was measured following the administration of [125I]-labelled PGE2 i.v. during fever induced by LPS, poly I:C, IL-1 or tumor necrosis factor alpha (TNF!). Both LPS and poly I:C stimulated an increase in plasma and CSF levels of PGE2 over a 5-h period with a peak at 60 min and 90 min, respectively, which occurred in parallel with the changes in body temperature. Ketoprofen abolished the rise in plasma and CSF PGE2 levels and the rise in body temperature in response to LPS, poly I:C and IL-1. In experiments where animals were given [125I]-labelled PGE2 i.v., radioactivity well above the background level was measured in samples of CSF collected from LPS-, poly I:C-, IL-1- or TNF!-pretreated animals. In contrast the radioactivity present in samples of CSF perfusate collected from control (saline-treated) animals was indistinguishable from the background level. These data indicate that cytokine inducers and cytokines increase the mass level of PGE2 in blood and CSF and also increases the entry, from the peripheral circulation, of radiolabelled PGE2 into the third cerebral ventricle.