Journal
NEUROBIOLOGY OF DISEASE
Volume 27, Issue 2, Pages 151-163Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.nbd.2007.04.013
Keywords
adenovirus; rat; IL-1 beta; brain; acute phase response; behaviour and injury
Categories
Funding
- MRC [G0300456] Funding Source: UKRI
- Medical Research Council [G0300456] Funding Source: researchfish
- Medical Research Council [G0300456] Funding Source: Medline
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Acute brain injury induces early and transient hepatic expression of chemokines, which amplify the injury response and give rise to movement of leukocytes into the blood and subsequently the brain and liver. Here, we sought to determine whether an ongoing injury stimulus within the brain would continue to drive the hepatic chemokine response and how it impacts on behaviour and CNS integrity. We generated chronic IL-1 beta expression in rat brain by adenoviral-mediated gene transfer, which resulted in chronic leukocyte recruitment, axonal injury and prolonged depression of spontaneous behaviour. IL-1 beta could not be detected in circulating blood, but a chronic systemic response was established, including extended production of hepatic and circulating chemokines, leukocytosis, liver damage, weight loss, decreased serum albumin and marked liver leukocyte recruitment. Thus, hepatic chemokine synthesis is a feature of active chronic CNS disease and provides an accessible target for the suppression of CNS inflammation. (c) 2007 Elsevier Inc. All rights reserved.
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