Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

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-1beta expression in rat brain by adenoviral-mediated gene transfer, which resulted in chronic leukocyte recruitment, axonal injury and prolonged depression of spontaneous behaviour. IL-1beta 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.

Original publication

DOI

10.1016/j.nbd.2007.04.013

Type

Journal article

Journal

Neurobiol Dis

Publication Date

08/2007

Volume

27

Pages

151 - 163

Keywords

Adenoviridae, Animals, Axons, Behavior, Animal, Blood-Brain Barrier, Brain, Brain Injuries, Chemokines, Chronic Disease, Enzyme-Linked Immunosorbent Assay, Gene Transfer Techniques, Immunohistochemistry, Inflammation, Interleukin-1beta, Liver, Motor Activity, Rats, Reverse Transcriptase Polymerase Chain Reaction