Journal
NEUROSCIENCE LETTERS
Volume 448, Issue 1, Pages 41-46Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2008.09.081
Keywords
Blood-brain barrier; Macrophages; Lipopolysaccharide; Cytokines; Inflammation
Categories
Funding
- EU [QLG3-Cr2002-00612]
- EU COST Action [BM0603]
- MS Society Grant [784/03]
Ask authors/readers for more resources
Systemic inflammation induces cytokine synthesis within the central nervous system. This results in sickness behaviour and may exacerbate ongoing neuroinflammatory disease. The precise mechanisms underlying the relay of signal from the periphery to the central nervous system are not entirely understood. CD163-positive macrophages occupy a unique position at the blood-brain barrier and upregulate prostaglandin-synthesizing enzymes in response to systemic inflammation. This finding suggests that they might play a role in signalling inflammation to the central nervous system. However, here we demonstrate that de novo brain cytokine transcription during systemic endotoxaemia may be prostaglandin-independent. We therefore set out to interrogate more directly the role of CD163-positive macrophages in immune-to-brain signalling. Intracerebroventricular injections of clodronate liposomes were used to selectively deplete CD163-positive macrophages. We show that de novo brain cytokine synthesis during systemic endotoxaemia persists in the absence of CD163-positive macrophages. Cerebral endothelial cells outnumber CD163-positive macrophages and are arguably better situated to signal circulating inflammatory stimuli to the brain. (c) 2008 Elsevier Ireland Ltd. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available