Monica Ek, David Engblom, Sipra Saha, Anders Blomqvist, Per-Johan Jakobsson & Anders Ericsson-Dahlstrand
Nature, 2001 March 22; 410, 430-431 (2001)
DOI: https://doi.org/10.1038/35068632
Abstract
Inflammatory reactions against invaders in the body call upon cytokine molecules that elicit systemic responses, such as fever, fatigue, increased pain sensitivity and appetite loss, mediated by the central nervous system. But how cytokines can induce these effects has been a mystery as they are unlikely to cross the blood–brain barrier1,2,3. Here we show that cerebral vascular cells express components enabling a blood-borne cytokine to stimulate the production of prostaglandin E2, an inflammatory mediator whose small size and lipophilic properties allow it to diffuse into the brain parenchyma. As receptors for this prostaglandin are found on responsive deep neural structures4,5,6, we propose that the activated immune system controls central reactions to peripheral inflammation through a prostaglandin-dependent, cytokine-mediated pathway.
