Chlamydial Manipulation of Host Apoptosis

衣原体操纵宿主细胞凋亡的机制 人类的衣原体感染对发育中和发育中的人都是一个主要的健康问题。 发达国家。泌尿生殖道C.沙眼是导致 性传播细菌疾病，也与某些类型的宫颈癌有关，而呼吸道感染C。肺炎菌与动脉粥样硬化有关，动脉粥样硬化是导致心脑血管死亡的主要血管疾病。虽然C.鹦鹉热主要是一种动物病原体，人类也容易感染鹦鹉热。鹦鹉热感染，发展成危及生命的肺炎。由于人类可以通过被C.鹦鹉热生物，CDC曾将C.作为生物防御的B类药剂。这些衣原体诱导的或相关的病理主要是由于衣原体的能力，无论是生产性复制或实现一个长期的持久性内的真核细胞的胞质空泡，这是由衣原体独特的细胞内双相生命周期和衣原体的能力，以逃避宿主防御的帮助。目前的建议是为了了解衣原体如何逃避一个非常重要的宿主防御效应机制-凋亡。我们以前已经证明，衣原体具有强大的抗细胞凋亡活性，这可能有助于衣原体的能力，在感染的宿主中存活很长一段时间。通过鉴定负责衣原体抗凋亡活性的分子并了解抗凋亡分子如何工作，如在当前项目中提出的，我们可能能够开发用于阻断衣原体抗凋亡活性和预防衣原体诱导的病理的试剂/方法。

Mechanisms of Chlamydial Manipulation of Host Cell Apoptosis Chlamydial infection in humans imposes a major health problem in both developing and developed nations. Urogenital tract infection with C. trachomatis species is a leading cause of sexually transmitted bacterial diseases and is also linked to certain type of cervical carcinoma while respiratory infection with C. pneumoniae species is associated with atherosclerosis, a major vascular condition for cardio-cerebral fatality. Although the species C. psittaci is primarily an animal pathogen, humans are also susceptible to C. psittaci infection, developing life-threatening pneumonia. Since humans can acquire infection via aerosolized animal feces that are contaminated with C. psittaci organisms, CDC has once listed C. psittaci as a category B agent for biodefense. These chlamydia-induced or -associated pathologies are largely due to chlamydial ability to either productively replicate or to achieve a long-term persistence within a cytoplasmic vacuole of eukaryotic cells, which are aided by the chlamydial unique intracellular biphasic life cycle and the chlamydial ability to evade host defense. The current proposal is designed to understand how chlamydia evades a very important host defense effector mechanism---apoptosis. We have previously demonstrated that chlamydia possesses a potent antiapoptotic activity, which may contribute to the chlamydial ability to survive in the infected hosts for long periods of time. By identifying the molecule(s) responsible for the chlamydial antiapoptotic activity and understanding how the antiapoptotic molecules work as proposed in the current project, we may be able to develop reagents/approaches for blocking the chlamydial antiapoptotic activity and preventing chlamydia-induced pathologies.