Chlamydia pneumoniae induces Alzheimer-like amyloid plaques in brains of BALB/c mice

被引:175
作者
Little, CS
Hammond, CJ
MacIntyre, A
Balin, BJ
Appelt, DM
机构
[1] Philadelphia Coll Osteopath Med, Dept Pathol Microbiol & Immunol, Philadelphia, PA 19131 USA
[2] Philadelphia Coll Osteopath Med, Dept Biomed Sci, Philadelphia, PA 19131 USA
关键词
Alzheimer's disease; amyloid; animal model; bacteria; Chlamylophila (Chlamydia) pneumoniae; infection; mouse; non-transgenic; olfactory; plaque; sporadic AD;
D O I
10.1016/S0197-4580(03)00127-1
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
03 ; 0303 ; 100203 ;
摘要
Amyloid deposits resembling plaques found in Alzheimer's disease (AD) brains were formed in the brains of non-transgenic BALB/c mice following intranasal infection with Chlamydia pneumoniae. The mice were infected at 3 months of age with C pneumoniae isolated from an AD brain. Infection was confirmed by light and electron microscopy in olfactory tissues of the mice. C pneumoniae was still evident in these tissues 3 months after the initial infection indicating that a persistent infection had been established. Amyloid beta (Abeta) 1-42 immunoreactive deposits were identified in the brains of infected BALB/c mice up to 3 months post-infection with the density, size, and number of deposits increasing as the infection progressed. A subset of deposits exhibited thioflavin-s labeling. Intracellular Abeta1-42 labeling was observed in neuronal cells. Experimental induction of amyloid deposition in brains of non-transgenic BALB/c mice following infection with C pneumoniae may be a useful model for furthering our understanding of mechanisms, linked to infection, involved in the initiation of the pathogenesis of sporadic AD. (C) 2003 Elsevier Inc. All rights reserved.
引用
收藏
页码:419 / 429
页数:11
相关论文
共 42 条
[31]  
Ossewaarde JM, 2000, P 4 M EUR SOC CHLAM
[32]   Failure to detect Chlamydia pneumoniae in the late-onset Alzheimer's brain [J].
Ring, RH ;
Lyons, JM .
JOURNAL OF CLINICAL MICROBIOLOGY, 2000, 38 (07) :2591-2594
[33]  
Rosen G.D., 2000, INT MOUSE GENOME C, V14, P166
[34]   Apolipoprotein E alleles as risk factors in Alzheimer's disease [J].
Roses, AD .
ANNUAL REVIEW OF MEDICINE, 1996, 47 :387-400
[35]  
Rottenberg ME, 1999, J IMMUNOL, V162, P2829
[36]   Two amyloid precursor protein transgenic mouse models with Alzheimer disease-like pathology [J].
SturchlerPierrat, C ;
Abramowski, D ;
Duke, M ;
Wiederhold, KH ;
Mistl, C ;
Rothacher, S ;
Ledermann, B ;
Burki, K ;
Frey, P ;
Paganetti, PA ;
Waridel, C ;
Calhoun, ME ;
Jucker, M ;
Probst, A ;
Staufenbiel, M ;
Sommer, B .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1997, 94 (24) :13287-13292
[37]   The gene defects responsible for familial Alzheimer's disease [J].
Tanzi, RE ;
Kovacs, DM ;
Kim, TW ;
Moir, RD ;
Guenette, SY ;
Wasco, W .
NEUROBIOLOGY OF DISEASE, 1996, 3 (03) :159-168
[38]  
Williams RW, 2000, RES PRO CEL, V30, P21
[39]   Intracellular APP processing and Aβ production in Alzheimer disease [J].
Wilson, CA ;
Doms, RW ;
Lee, VMY .
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY, 1999, 58 (08) :787-794
[40]   Intraneuronal APP/Aβ trafficking and plaque formation in β-amyloid precursor protein and presenilin-1 transgenic mice [J].
Wirths, O ;
Multhaup, G ;
Czech, C ;
Feldmann, N ;
Blanchard, V ;
Tremp, G ;
Beyreuther, K ;
Pradier, L ;
Bayer, TA .
BRAIN PATHOLOGY, 2002, 12 (03) :275-286