Detection of amyloid beta aggregates in the brain of BALB/c mice after Chlamydia pneumoniae infection

• Published in: Acta neuropathologica Vol. 114; no. 3; pp. 255 - 261
• Main Authors: Boelen, Ellen, Stassen, Frank R M, van der Ven, André J A M, Lemmens, Marijke A M, Steinbusch, Hellen P J, Bruggeman, Cathrien A, Schmitz, Christoph, Steinbusch, Harry W M
• Format: Journal Article
• Language: English
• Published: Germany Springer Nature B.V 01-09-2007; Springer-Verlag
• Subjects: Alzheimer's disease; Amyloid beta-Peptides - metabolism; Amyloid beta-Protein Precursor - genetics; Animals; Brain; Brain - microbiology; Brain - pathology; Chlamydia; Chlamydophila Infections - pathology; Chlamydophila pneumoniae; Disease; Female; Humans; Immunohistochemistry; Infections; Mice; Mice, Inbred BALB C; Mice, Transgenic; Microscopy, Confocal; Mutation; Neurodegenerative Diseases - microbiology; Original Paper; Pathogenesis; Pathogens; Pathology; Peptide Fragments - genetics; Plaque, Amyloid - parasitology; Proteins; Reverse Transcriptase Polymerase Chain Reaction; Netherlands
• ISSN: 0001-6322; 1432-0533
• DOI: 10.1007/s00401-007-0252-3

Neuroinflammation, initiated by cerebral infection, is increasingly postulated as an aetiological factor in neurodegenerative diseases such as Alzheimer's disease (AD). We investigated whether Chlamydia pneumoniae (Cpn) infection results in extracellular aggregation of amyloid beta (Abeta) in BALB/c mice. At 1 week post intranasal infection (p.i.), Cpn DNA was detected predominantly in the olfactory bulbs by PCR, whereas brains at 1 and 3 months p.i. were Cpn negative. At 1 and 3 months p.i., extracellular Abeta immunoreactivity was detected in the brain of Cpn-infected mice but also in the brain of mock-infected mice and mice that were neither Cpn infected nor mock infected. However, these extracellular Abeta aggregates showed morphological differences compared to extracellular Abeta aggregates detected in the brain of transgenic APP751(SL)/PS1(M146L) mice. These data do not unequivocally support the hypothesis that Cpn infection induces the formation of AD-like Abeta plaques in the brain of BALB/c mice, as suggested before. However, future studies are required to resolve these differences and to investigate whether Cpn is indeed an etiological factor in AD pathogenesis.