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Chlamydia pneumoniae and age-related macular degeneration: a role in pathogenesis or merely a chance association?

机译:肺炎衣原体和年龄相关性黄斑变性:在发病机制中起作用还是仅仅是偶然性联系?

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The role of inflammation in the aetiology of age-related macular degeneration (AMD) has become very topical as the discovery that genetic variation in complement pathway genes influences the risk of developing AMD. Complement factor H gene, an inhibitor of the alternative complement activation pathway along with other complement pathway genes factor F (BF) and C2 show significant contribution to the risk of AMD. The alternative complement pathway is activated by a trigger, which is often microbial in nature. One current model of AMD aetiology implicates aberrant regulation of the alternative pathway of complement, in combination with some unknown infectious agents. Chlamydia pneumoniae could be one such potential trigger of the alternative complement pathway and several investigations have linked C. pneumoniae to AMD. However, there are only a few studies to date and numbers in most studies are small. Also there are many difficulties in verifying laboratory techniques for the detection of C. pneumoniaechronic infection. As such we need to be cautious not to over interpret the current results. However, the findings certainly give impetus for further work on C. pneumoniae and AMD. This paper provides an overview of work in this area.
机译:由于发现补体途径基因的遗传变异会影响罹患AMD的风险,因此炎症在与年龄相关的黄斑变性(AMD)的病因中的作用已成为非常热门的话题。补体因子H基因(一种替代性补体激活途径的抑制剂)与其他补体途径基因的因子F(BF)和C2一起,对AMD的风险具有重要作用。备选补体途径由触发器触发,触发器通常是微生物。当前的AMD病因学模型涉及与一些未知的传染原结合对补体替代途径的异常调节。肺炎衣原体可能是替代补体途径的这种潜在触发因素,一些研究已将肺炎衣原体与AMD联系起来。但是,迄今为止只有很少的研究,并且大多数研究中的数字都很小。在验证用于检测肺炎衣原体慢性感染的实验室技术方面也存在许多困难。因此,我们需要谨慎,不要过度解释当前的结果。但是,这些发现无疑为进一步开展肺炎衣原体和AMD的研究提供了动力。本文概述了该领域的工作。

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