Chlamydia pneumoniae infection enhances microglial activation in atherosclerotic mice

Voorend, M.; van der Ven, A.J.A.M.; Mulder, M.; Lodder, J.; Steinbusch, H.W.M.; Bruggeman, C.A.

doi:10.1016/j.neurobiolaging.2008.09.022

« Previous Next »Neurobiology of Aging
Volume 31, Issue 10 , Pages 1766-1773, October 2010

Chlamydia pneumoniae infection enhances microglial activation in atherosclerotic mice

M. Voorend
- Department of Neurology, Cardiovascular Research Institute Maastricht (CARIM), University Hospital Maastricht, the Netherlands
- Corresponding author at: Department of Neurology, University Hospital Maastricht, PO Box 5800, 6202 AZ Maastricht, Netherlands. Tel.: +31 43 3875061; fax: +31 43 3877055.
A.J.A.M. van der Ven
- Department of Internal Medicine, University Hospital Nijmegen, the Netherlands
M. Mulder
- European Graduate School of Neuroscience (EURON), the Netherlands
- Department of Genetics and Molecular Cellbiology, the Netherlands
J. Lodder
- Department of Neurology, Cardiovascular Research Institute Maastricht (CARIM), University Hospital Maastricht, the Netherlands
H.W.M. Steinbusch
- Department of Psychiatry and Neuropsychology, the Netherlands
- European Graduate School of Neuroscience (EURON), the Netherlands
C.A. Bruggeman
- Department of Medical Microbiology, Cardiovascular Research Institute Maastricht (CARIM), University Hospital Maastricht, the Netherlands

Received 16 October 2006; received in revised form 14 September 2008; accepted 30 September 2008. published online 25 November 2008.

Abstract

The presence of Chlamydia pneumoniae in murine brain tissue was studied in atherosclerotic and non-atherosclerotic mice, after peritoneal injection. Furthermore, we investigated whether increased permeability of the blood–brain barrier was implicated in cerebral C. pneumoniae infection and whether intra-cerebral C. pneumoniae infection leads to microglial activation. Using a polymerase chain reaction, C. pneumoniae DNA was found in the brain tissue of 33% of the mice, 3, 7 and 21 days after infection. Atherosclerosis and age does not influence the extend of the cerebral infection. Semiquantitative analyses showed that intra-cerebral C. pneumoniae infection was not accompanied by an altered function of the blood–brain barrier. Microglial activation was assessed with immunohistochemistry, quantified in the hippocampus of each infected mouse and compared with mock infected. Enhanced microglial activation was found in the atherosclerotic mice. Since microglial activation is a key factor in a number of neuroinflammatory diseases, C. pneumoniae infection might play a role in these diseases.

Keywords: Chlamydia pneumoniae, Atherosclerosis, Blood–brain barrier, Microglial activation, Neuroinflammatory disorders