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Brain Advance Access published online on August 3, 2006
Brain, doi:10.1093/brain/awl206
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© The Author (2006). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Received February 8, 2006
Revised June 30, 2006
Accepted July 5, 2006

Article

Circulating monocytes engraft in the brain, differentiate into microglia and contribute to the pathology following meningitis in mice

Marija Djukic 1, Alexander Mildner 2, Hauke Schmidt 2, Dirk Czesnik 3, Wolfgang Brück 2, Josef Priller 4, Roland Nau 1 *, and Marco Prinz 2 * *

1 Department of Neurology, Georg August University, Göttingen, Germany
2 Institute of Neuropathology, Georg August University, Göttingen, Germany
3 Department of Neurophysiology and Cellular Biophysics, Institute of Physiology and Pathophysiology, Georg August University, Göttingen, Germany
4 Department of Psychiatry, Charité-Universitätsmedizin Berlin, Berlin, Germany; Department of Experimental Neurology, Charité-Universitätsmedizin Berlin, Berlin, Germany

* To whom correspondence should be addressed.
Marco Prinz, E-mail: mprinz{at}med.uni-goettingen.de


  Abstract

Previous studies have demonstrated a potential role of brain endogenous microglia and meningeal macrophages in inflammation and brain injury during bacterial meningitis. However, the contribution of previously engrafted monocytes and microglia to this process is still unknown. We therefore used genetically labelled bone marrow-derived cells from transgenic mice expressing the green fluorescent protein (GFP) under the chicken {beta}-actin promoter to deliver fluorescently labelled monocytes to the diseased brain. Approximately 24 hours after Streptococcus pneumoniae infection, GFP-expressing parenchymal microglia changed their morphology to an activated phenotype and upregulated major histocompatibility complex class II molecules. Bacterial meningitis increased the engraftment of GFP+ monocytes and their differentiation to microglia during the post-inflammatory period, but not during acute meningitis. Importantly, these newly recruited monocytes became an integral part of the pool of parenchymal microglia and contributed to the clearance of damaged tissue by increased lysosomal activity and close location to apoptotic cells. Thus, circulating cells entering the brain such as monocytes/macrophages might provide a potential cellular target for the treatment of the tissue damage following meningitis via peripheral cell therapy.

Keywords: GFP chimeras; meningitis; microglia turnover; S. pneumoniae.
*These authors have contributed equally to this work.
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