Pathology/Microbiology/Immunology and Forensic Medicine Department, Philadelphia College of Osteopathic Medicine, 4170 City Ave, Philadelphia, Pennsylvania, USA.
BMC Neurosci. 2010 Sep 23;11:121. doi: 10.1186/1471-2202-11-121.
Sporadic late-onset Alzheimer's disease (AD) appears to evolve from an interplay between genetic and environmental factors. One environmental factor that continues to be of great interest is that of Chlamydia pneumoniae infection and its association with late-onset disease. Detection of this organism in clinical and autopsy samples has proved challenging using a variety of molecular and histological techniques. Our current investigation utilized immunohistochemistry with a battery of commercially available anti-C. pneumoniae antibodies to determine whether C. pneumoniae was present in areas typically associated with AD neuropathology from 5 AD and 5 non-AD control brains.
Immunoreactivity for C. pneumoniae antigens was observed both intracellularly in neurons, neuroglia, endothelial cells, and peri-endothelial cells, and extracellularly in the frontal and temporal cortices of the AD brain with multiple C. pneumoniae-specific antibodies. This immunoreactivity was seen in regions of amyloid deposition as revealed by immunolabeling with two different anti-beta amyloid antibodies. Thioflavin S staining, overlaid with C. pneumoniae immunolabeling, demonstrated no direct co-localization of the organism and amyloid plaques. Further, the specificity of C. pneumoniae labeling of AD brain sections was demonstrated using C. pneumoniae antibodies pre-absorbed against amyloid β 1-40 and 1-42 peptides.
Anti-C. pneumoniae antibodies, obtained commercially, identified both typical intracellular and atypical extracellular C. pneumoniae antigens in frontal and temporal cortices of the AD brain. C. pneumoniae, amyloid deposits, and neurofibrillary tangles were present in the same regions of the brain in apposition to one another. Although additional studies are required to conclusively characterize the nature of Chlamydial immunoreactivity in the AD brain, these results further implicate C. pneumoniae infection with the pathogenesis of Alzheimer's disease.
散发性迟发性阿尔茨海默病（AD）似乎是由遗传和环境因素相互作用引起的。环境因素中，衣原体肺炎感染及其与迟发性疾病的关联一直是人们关注的焦点。使用各种分子和组织学技术，在临床和尸检样本中检测到该病原体一直具有挑战性。我们目前的研究利用免疫组织化学技术，使用一系列市售的抗衣原体肺炎抗体，从 5 例 AD 和 5 例非 AD 对照大脑中与 AD 神经病理学相关的典型区域确定是否存在衣原体肺炎。
用多种针对衣原体肺炎的特异性抗体，在 AD 大脑的额颞叶皮质中观察到神经元、神经胶质细胞、内皮细胞和内皮细胞周围细胞的细胞内和细胞外衣原体肺炎抗原的免疫反应性。这种免疫反应性在用两种不同的抗β淀粉样蛋白抗体免疫标记的淀粉样沉积区域可见。用硫黄素 S 染色，与衣原体肺炎免疫标记重叠，未显示该生物体与淀粉样斑块的直接共定位。此外，使用预吸附针对淀粉样β 1-40 和 1-42 肽的衣原体肺炎抗体，证明了 AD 脑切片中衣原体肺炎标记的特异性。
商业获得的抗衣原体肺炎抗体鉴定了 AD 大脑额颞叶皮质中典型的细胞内和非典型的细胞外衣原体肺炎抗原。衣原体肺炎、淀粉样沉积物和神经原纤维缠结存在于大脑的同一区域，彼此相邻。尽管还需要进一步的研究来明确表征 AD 大脑中衣原体免疫反应的性质，但这些结果进一步表明衣原体肺炎感染与阿尔茨海默病的发病机制有关。
