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Analysis of AB 1‐42 amyloid in neuronal cells infected with Herpes Simplex Virus 1 and Chlamydophila (Chlamydia) pneumoniae
Author(s) -
Triplett Laura Rebecca,
Kralik Kevin Scott,
Balin Brian Joseph,
Hingley Susan Tuttle,
Appelt Denah Marie
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.lb67-b
Subject(s) - chlamydophila pneumoniae , immunolabeling , pathogen , herpes simplex virus , chlamydia , biology , virology , immunocytochemistry , virus , amyloid (mycology) , immunology , chlamydiaceae , microbiology and biotechnology , pathology , medicine , immunohistochemistry , botany , endocrinology
Several studies have suggested an infectious etiology for Alzheimer’s disease (AD). Previously, our laboratory identified Chlamydia pneumoniae (Cpn) from autopsied sporadic AD brains as well as developed a BALB/c mouse model that demonstrated infection‐induced amyloid plaques similar to those found in AD. An additional pathogen, herpes simplex virus type 1 (HSV1), has been implicated in AD, possibly by triggering processing of the beta amyloid precursor protein (βAPP), thereby contributing to amyloid plaque formation. Our current study examines infection of the SK‐N‐MC human neuronal cells with Cpn and HSV1 with regards to amyloid processing. Immunocytochemistry was used to analyze the outcome of infection by these two pathogens. Following a 72 hr Cpn infection of the cells, an increase in cytoplasmic labeling of Aβ 1‐42 was observed relative to uninfected cells; an apparent increase in nuclear labeling of Aβ 1‐42 was observed following HSV1 infection. In contrast, co‐infections with Cpn and HSV1 resulted in decreased levels of Aβ 1‐42 labeling when compared to infection with a single pathogen. These data suggest that infection of neuronal cells by individual pathogens may modify processing of βAPP resulting in Aβ 1‐42 immunolabeling. However, co‐infection resulted in reduced labeling, thereby suggesting that one pathogen can interfere with another in inducing Aβ 1‐42 immunoreactivity.