Inhibition of apoptosis in neuronal cells infected with Chlamydophila (Chlamydia) pneumoniae
1 Department of Neuroscience, Physiology & Pharmacology, Philadelphia College of Osteopathic Medicine, Philadelphia, USA
2 Department of Pathology, Microbiology & Immunology, Philadelphia College of Osteopathic Medicine, Philadelphia, USA
3 Center for Chronic Disorders of Aging; Philadelphia College of Osteopathic Medicine, Philadelphia, USA
Citation and License
BMC Neuroscience 2008, 9:13 doi:10.1186/1471-2202-9-13Published: 24 January 2008
Chlamydophila (Chlamydia) pneumoniae is an intracellular bacterium that has been identified within cells in areas of neuropathology found in Alzheimer disease (AD), including endothelia, glia, and neurons. Depending on the cell type of the host, infection by C. pneumoniae has been shown to influence apoptotic pathways in both pro- and anti-apoptotic fashions. We have hypothesized that persistent chlamydial infection of neurons may be an important mediator of the characteristic neuropathology observed in AD brains. Chronic and/or persistent infection of neuronal cells with C. pneumoniae in the AD brain may affect apoptosis in cells containing chlamydial inclusions.
SK-N-MC neuroblastoma cells were infected with the respiratory strain of C. pneumoniae, AR39 at an MOI of 1. Following infection, the cells were either untreated or treated with staurosporine and then examined for apoptosis by labeling for nuclear fragmentation, caspase activity, and membrane inversion as indicated by annexin V staining. C. pneumoniae infection was maintained through 10 days post-infection. At 3 and 10 days post-infection, the infected cell cultures appeared to inhibit or were resistant to the apoptotic process when induced by staurosporine. This inhibition was demonstrated quantitatively by nuclear profile counts and caspase 3/7 activity measurements.
These data suggest that C. pneumoniae can sustain a chronic infection in neuronal cells by interfering with apoptosis, which may contribute to chronic inflammation in the AD brain.