News Embargo:
All information contained here is
embargoed for release until the
date and time of presentation at the
Conference, unless written notice of
change of date/time is provided in
advance by the Alzheimer's Association.
Any questions can be directed to:
Niles Frantz
Associate Director, Public Relations
Alzheimer’s Association
312-335-5777
niles.frantz@alz.org
|
|
| The Effects of the Chlamydia Pneumoniae Infectious Process on Neuronal Cells: Implications for Alzheimer’s Disease |
| Topic:
Molecular Mechanisms of Neurodegeneration - Apoptosis |
| Denah M. Appelt, Maria Roupas, Christine J. Hammond, Christopher S. Little, Brian J. Balin, Philadelphia College of Osteopathic Medicine, Philadelphia, PA, USA. Contact e-mail: DenahA@pcom.edu |
| Presentation Number: P3-189 |
| Keyword:
apoptosis, infectious disease, neuropathology |
Background: Chlamydia pneumoniae has been implicated in the pathogenesis of Alzheimer’s disease (AD). While controversial, the focus of this study is the relationship between infection and neurodegeneration. Typically, obligate intracellular organisms, such as C. pneumoniae, if not cleared by the immune system will evoke an apoptotic process of the infected cell. Intriguingly, it has been demonstrated that infection with C. pneumoniae, of monocytes and epithelial cells, inhibits the apoptotic process.
Objective(s): The importance of this work may be the correlation of infection with the apoptotic process observed in AD. The apoptotic process in AD has been shown to be initiated although there is debate whether it goes to completion. Our current study with infection in neuronal cells may provide insight into this process.
Methods: In this current study, SK-N-MC neuroblastoma cells were infected with C. pneumoniae followed by the addition of staurosporine to induce apoptosis. These cells were monitored for apoptotic changes by immunocytochemistry, immunoblotting, and electron microscopy.
Results: Our earlier studies found that human monocytes, endothelia, and glia infected with C. pneumoniae demonstrated increased production and processing of amyloid (Aβ) 1-42; and yet, both proinflammatory molecules and Aβ 1-42 have been shown to induce apoptosis in neuronal cells in vitro. Hence, an infection with C. pneumoniae may inhibit the apoptotic process while promoting a buildup of Aβ within neuronal cells. In our novel murine model in which we infected non-transgenic mice with C. pneumoniae, we found deposits of Aβ in areas of the brain most affected in AD. The neurons in these areas showed intracellular Aβ 1-42 immunoreactivity and these neurons did not appear to be apoptotic. Our results showed that both neuronal cells directly infected with C. pneumoniae and uninfected neighboring cells, in close contact, were less vulnerable to apoptosis. A persistent infection was maintained, in this paradigm, for up to three months.
Conclusions: Inhibition of apoptosis may be one mechanism by which C. pneumoniae can sustain an infection in the host to maintain an optimal intracellular environment. This cumulative data will further our knowledge into the relationship between infection and apoptosis in the pathogenesis of AD. |
| Commercial Relationship: D.M. Appelt, None. |
| |
|
|
|
|
|
|
|
|
The Online Abstract Submission and Invitation System
© 1996 - 2010 Coe-Truman Technologies, Inc. All rights reserved.
|
|
|
|
|
|
