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Open Access Highly Accessed Methodology article

Immunohistological detection of Chlamydia pneumoniae in the Alzheimer's disease brain

Christine J Hammond13, Loretta R Hallock1, Raymond J Howanski1, Denah M Appelt23, C Scott Little13 and Brian J Balin13*

Author Affiliations

1 Pathology/Microbiology/Immunology and Forensic Medicine Department, Philadelphia College of Osteopathic Medicine, 4170 City Ave, Philadelphia, Pennsylvania, USA

2 Neuroscience/Physiology/Pharmacology Department, Philadelphia College of Osteopathic Medicine, 4170 City Ave, Philadelphia, Pennsylvania, USA

3 Center for Chronic Disorders of Aging, Philadelphia College of Osteopathic Medicine, 4170 City Ave, Philadelphia, Pennsylvania, USA

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BMC Neuroscience 2010, 11:121  doi:10.1186/1471-2202-11-121

Published: 23 September 2010

Abstract

Background

Sporadic late-onset Alzheimer's disease (AD) appears to evolve from an interplay between genetic and environmental factors. One environmental factor that continues to be of great interest is that of Chlamydia pneumoniae infection and its association with late-onset disease. Detection of this organism in clinical and autopsy samples has proved challenging using a variety of molecular and histological techniques. Our current investigation utilized immunohistochemistry with a battery of commercially available anti-C. pneumoniae antibodies to determine whether C. pneumoniae was present in areas typically associated with AD neuropathology from 5 AD and 5 non-AD control brains.

Results

Immunoreactivity for C. pneumoniae antigens was observed both intracellularly in neurons, neuroglia, endothelial cells, and peri-endothelial cells, and extracellularly in the frontal and temporal cortices of the AD brain with multiple C. pneumoniae-specific antibodies. This immunoreactivity was seen in regions of amyloid deposition as revealed by immunolabeling with two different anti-beta amyloid antibodies. Thioflavin S staining, overlaid with C. pneumoniae immunolabeling, demonstrated no direct co-localization of the organism and amyloid plaques. Further, the specificity of C. pneumoniae labeling of AD brain sections was demonstrated using C. pneumoniae antibodies pre-absorbed against amyloid β 1-40 and 1-42 peptides.

Conclusions

Anti-C. pneumoniae antibodies, obtained commercially, identified both typical intracellular and atypical extracellular C. pneumoniae antigens in frontal and temporal cortices of the AD brain. C. pneumoniae, amyloid deposits, and neurofibrillary tangles were present in the same regions of the brain in apposition to one another. Although additional studies are required to conclusively characterize the nature of Chlamydial immunoreactivity in the AD brain, these results further implicate C. pneumoniae infection with the pathogenesis of Alzheimer's disease.