Chlamydia pneumoniae infection enhances microglial activation in atherosclerotic mice

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

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

3 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)1766-1773
Number of pages8
JournalNeurobiology of Aging
Issue number10
Publication statusPublished - Oct 2010

Bibliographical note

Funding Information:
The research described in this manuscript was funded by a grant from the Netherlands Heart Foundation, grant number 99-134.


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