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Updated: Jun 27, 2026
A Mouse Model for Pathogen-induced Chronic Inflammation at Local and Systemic Sites
Published on: August 8, 2014
Chlamydia pneumoniae infection enhances microglial activation in atherosclerotic mice
M Voorend1, A J A M van der Ven, M Mulder
1Department of Neurology, Cardiovascular Research Institute Maastricht (CARIM), University Hospital Maastricht, the Netherlands. manuelavoorend@gmail.com
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.
Insights
Chlamydia pneumoniae infection was detected in mouse brains, independent of atherosclerosis. However, atherosclerotic mice showed increased microglial activation, suggesting a potential role for this infection in neuroinflammatory diseases.
Area of Science:
- Neuroscience
- Infectious Diseases
- Immunology
Background:
- Chlamydia pneumoniae is a bacterium linked to various chronic conditions.
- Its presence and effects within the central nervous system, particularly in the context of atherosclerosis, are not fully understood.
- Microglial activation is a critical component of neuroinflammation.
Purpose of the Study:
- To determine the presence of Chlamydia pneumoniae in murine brain tissue.
- To investigate the association between cerebral Chlamydia pneumoniae infection and blood-brain barrier permeability.
- To assess whether intra-cerebral Chlamydia pneumoniae infection induces microglial activation, especially in atherosclerotic models.
Main Methods:
- Mice (atherosclerotic and non-atherosclerotic) were intraperitoneally injected with Chlamydia pneumoniae.
- Polymerase chain reaction (PCR) was used to detect Chlamydia pneumoniae DNA in brain tissue at 3, 7, and 21 days post-infection.
- Blood-brain barrier function was assessed using semiquantitative analyses.
- Microglial activation was evaluated via immunohistochemistry in the hippocampus.
Main Results:
- Chlamydia pneumoniae DNA was detected in the brain tissue of 33% of infected mice.
- Cerebral infection prevalence was not influenced by atherosclerosis or age.
- Intra-cerebral Chlamydia pneumoniae infection did not alter blood-brain barrier function.
- Enhanced microglial activation was observed in atherosclerotic mice following infection.
Conclusions:
- Chlamydia pneumoniae can establish infection within the murine brain.
- While not affecting blood-brain barrier integrity, the infection is associated with microglial activation in atherosclerotic mice.
- These findings suggest a potential role for Chlamydia pneumoniae in neuroinflammatory processes and diseases.
