The objective of this study is to continue to investigate the role of infection as a possible risk factor for sporadic AD. Previous mouse models using Chlamydia pneumoniae (Cpn) demonstrated that intranasal inoculation with this organism can possibly induce AD-like pathology in mouse brain tissue. Studies have demonstrated that Chlamydia trachomatis (Ctr) can disseminate from its primary site of infection and plays a major role in the induction of reactive arthritis. The question our lab wanted to answer is whether Chlamydia muridarum (C. muridarum), can establish infection in the mouse brain tissue following intranasal inoculation and induce amyloid pathology. To answer this question non-transgenic BALB/c mouse were intranasallay inoculated with C. muridarum a mouse adapted respiratory isolate of Ctr. During the study, in vivo passaged C. muridarum and stock C. muridarum were utilized. Mouse brain tissue was examined at the 60 day time point p.i. for chlamydia specific labeling and amyloid pathology using immunohistochemistry techniques and visualized by brightfield microscopy. Analysis of the data at the 2 month time point indicated varying degrees chlamydia and amyloid pathology for both the in vivo passaged C. muridarum and the stock C. muridarum. However, the in vivo passage C. muridarum had a greater difference in both chlamydia specific labeling and amyloid deposition between the titer negative controls and titer positive experimentals over the stock C. muridarum. In addition, greater chlamydia antigen and amyloid pathology was observed in mice infected with Cpn AR-39 over both experimental C. muridarum groups. The data suggests that the degree of pathology induced following intranasal infection is dependent on the isolate of the organism introduced and that infection with C. muridarum was not as great of a stimulus for developing AD-like pathology as was infection with Cpn.
Available at: http://works.bepress.com/brian_balin/16/