Proof of Concept Studies of Chlamydia Pneumoniae Infection as a Trigger for Late-onset Alzheimer Disease

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Aims Objectives: Chronic infection(s) may be initiators for Alzheimer disease pathogenesis. Our laboratory has shown that Chlamydia pneumoniae infects cells in vitro, can survive intracellularly for long periods of time, and is detectable in Alzheimer disease brain tissues. Proof of concept studies are being performed to determine how infection may enter the brain, influence protein and gene regulation, and activate neuroinflammation observed in Alzheimer disease. Method Animal (BALB/c mice) and cellular studies are evaluating entry of Chlamydia pneumoniae into the brain and human monocytic cells, respectively, and the consequences of infection with regards to gene and protein expression. Proteins and genes involved with AD pathology and neuroinflammation are being analyzed using commercial human ELISA and qRTPCR Array approaches. Results Amyloid turn-on (Abeta 1-42) occurs in both animal brains and human cells following Chlamydia pneumoniae infection. Genes and proteins corresponding to neuroinflammatory markers and inflammasomes from infectied cells (eg, THP1 monocytes) are up-regulated when compared with uninfected monocytes. Of those genes and proteins up-regulated, CCL2, IL-1beta, AIM2, and IDO are significantly changed and reflect the activated pro-inflammatory state of infected monocytes. Conclusion Our data suggest that Chlamydia pneumoniae introduced intranasally to normal BALB/c mice triggers the accumulation of Abeta 1-42 in the brain. Further, upon infection of THP-1 monocytes, significant changes occur in the regulation of gene transcripts and protein expression that correlates to the inflammatory signature observed in late-onset Alzheimer disease. Thus, our data suggest that infection can trigger specific protein and gene changes that correlate to Alzheimer disease pathogenesis.

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Neurodegenerative Diseases




Supplement 1

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This abstract was published in Neurogenative Diseases, Volume 17, Supplement 1, Page 243.

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