Background and Significance: Previous studies have shown that cells infected with Chlamydia pneumoniae (Cpn) exhibit altered gene expression consistent with that observed in Alzheimer’s disease (AD). Furthermore, AD neurodegeneration has been linked to dysregulation of intracellular calcium and calcium-related processes. Therefore, we hypothesize that one mechanism by which pathogenesis evolves in AD is through infection-induced changes in expression of calcium-related genes. Objectives: To determine if infection of neuronal cells with Cpn alters expression of calciumrelated genes associated with neurodegeneration. Methods: SK-N-MC neuronal cells were infected with Cpn (AR39 strain; MOI=1) for 3 to 72 hours, then calcium-related genes were screened with real-time PCR microarrays (SABiosciences PAHS-066). Results: Following infection, approximately 29 genes displayed regulation changes of 2-fold or greater, including genes pertaining to neurotransmitters, cell cycle and immune regulators, and other calcium-responsive elements. Genes involved in synaptic function and memory such as AREG, ATF3, EGR2 and GEM were initially up regulated, then fell to baseline or below by 72 hours. Many of the affected genes have been implicated in AD pathogenesis. Conclusions: Our data suggest that Cpn alters calcium-related gene expression in host neurons consistent with calcium dysfunction previously documented in AD. This study may elucidate how, in its effort to establish a favorable environment, Cpn could affect cellular processes that contribute to AD pathogenesis.
Available at: http://works.bepress.com/susan_hingley/7/