Microbial Origins of Chronic Human Disease
人类慢性疾病的微生物起源
基本信息
- 批准号:6756919
- 负责人:
- 金额:$ 0.5万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2004
- 资助国家:美国
- 起止时间:2004-03-01 至 2005-02-28
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
DESCRIPTION (provided by applicant): Infection, inflammation, fever, and resumption of health (with or without antimicrobial treatment)--this is the common view of the pathological course of infectious diseases. However, it has become apparent over the years that the mechanisms of diseases associated with infectious pathogens, particularly chronic disorders, may be the end product of a multitude of pathogenesis pathways. Moreover, in many cases the infectious pathogens may vary, but the clinical consequences of the resulting inflammatory responses may lead to similar, if not identical, disease expression. Consider that infecting agents may produce chronic disease through a variety of mechanisms, besides by immediate, direct damage of infected cells. Pathogens may infect persistently--sometimes in apparent clinical silence--with evidence of disease arising many years later. Connection between the infection and the disease state may be abundantly apparent when a majority of infected individuals ultimately exhibit the diseases symptoms. However, when only a minority of those infected develop chronic disease symptoms the etiologic link between an infectious organism and the chronic disease symptoms may be harder to connect. Even when connections between persistent infection with an organism and a specific disease are firmly established confusion can arise when the disease association is restricted to only a few strains of a larger pathogen species. Sometimes an organism is difficult to recover or identify or is even not sought because an infectious etiology is not seriously considered. Further, in some cases even when the infection is transient and the organism is cleared, a chronic disease state can be left behind due to a variety of mechanisms, including autoimmunity due to immune mimicry. The value of the immune response in removing the infecting pathogen is clear; however, what is also clear is the delicate balance between effective and damaging--or immunopathogenic/immunological activity. With new diagnostic and investigative techniques available to identify previously unsuspected pathogens, we are poised scientifically to answer the diagnostic and mechanistic medical dilemmas that have been around for centuries surrounding the possibility of infectious causes of chronic diseases. However, it is important to develop a new and careful medico-research approach to this issue, to frame and ask the right questions, and to think creatively about how to answer these questions. It is also important to develop a sound experimental framework to approach this issue, combining the best of clinical medical approaches, clinical research studies, animal models, and basic research investigations. The American Academy of Microbiology plans to convene a colloquium on "Microbial Triggers of Chronic Illness" to address just these issues. The colloquium is scheduled for January 15-18, 2004 in Tucson, Arizona. A group of approximately 25 scientists, including the steering committee, will be invited to participate in this colloquium.
描述(由申请人提供):感染,炎症,发烧和健康恢复(有或没有抗菌治疗) - 这是感染疾病病理学病程的常见。然而,多年来,与传染病,尤其是慢性疾病相关的疾病机制可能是多种发病机理途径的最终产物。此外,在许多情况下,感染性病原体可能会有所不同,但是炎症反应的临床后果可能会导致相似的疾病表达,甚至可能导致相似的疾病表达。考虑到感染剂可以通过多种机制产生慢性疾病,除了直接损害感染细胞。病原体可能会持续感染 - 有时在明显的临床沉默中 - 有很多年后出现的疾病证据。当大多数感染者最终表现出疾病症状时,感染与疾病状态之间的联系可能很明显。但是,当只有少数被感染的人出现慢性疾病症状时,传染性生物与慢性疾病症状之间的病因学可能很难连接。即使持续感染与生物体与特定疾病之间的联系也会牢固地确定,当疾病关联仅限于仅几种较大的病原体种类的菌株时。有时,有机体很难恢复或识别,甚至不寻求,因为不认真考虑传染病学。此外,在某些情况下,即使感染是短暂的并且清除了生物体,由于各种机制,包括免疫模仿导致的自身免疫性,也可以遗留慢性疾病状态。免疫反应在去除感染病原体中的值很明显。但是,很明显的是有效和破坏性之间的微妙平衡 - 或免疫发病/免疫学活动。有了新的诊断和调查技术来识别先前未知的病原体,我们有理由科学地回答已经存在数百年历史的诊断和机械性困境,围绕感染性疾病的可能性。但是,重要的是要为此问题开发一种新的,仔细的医疗研究方法,构架和提出正确的问题,并创造性地思考如何回答这些问题。建立一个合理的实验框架来解决此问题也很重要,结合了最好的临床医学方法,临床研究,动物模型和基础研究研究。美国微生物学会计划召集有关“慢性病微生物触发因素”的座谈会,以解决这些问题。该座谈会定于2004年1月15日至18日在亚利桑那州图森市举行。包括指导委员会在内的大约25名科学家组成的小组将被邀请参加这次座谈会。
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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Ronald B Luftig其他文献
Ronald B Luftig的其他文献
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