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首页> 外文学位 >The alveolar macrophage in pulmonary infection- A comparison of permissiveness to infection with an obligate and a facultative intracellular pathogen.
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The alveolar macrophage in pulmonary infection- A comparison of permissiveness to infection with an obligate and a facultative intracellular pathogen.

机译：肺部感染中的肺泡巨噬细胞-与专性和兼性细胞内病原体感染的允许性比较。

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摘要

The lung must mount an effective immune response to pathogenic challenge while controlling attendant tissue damage. Central to this co-ordination are the immunomodulatory effects exerted by the pulmonary environment on the local alveolar macrophages (AMs). Moreover, intracellular pathogens are known to exploit the host immune system. For this reason, we hypothesized that the resident AM would comprise a vulnerable population of cells capable of being exploited by intracellular pathogens. To test this hypothesis, we investigated the role of the AM during pulmonary infection with either the obligate intracellular bacterium Coxiella burnetii or the facultative intracellular fungus Cryptococcus neoformans..;We showed [1] that resident AM are indeed the cell-type most susceptible to infection with C. burnetii. These resident AM remain infected up to twelve days, serving as a permissive niche that supports bacterial survival. Additionally, a subset of infected AMs underwent a characteristic phenotypic change in response to infection, resulting in an increased expression of surface integrin CD11b and continued expression of surface integrin CD11c. We conclude that C. burnetii is capable of exploiting the pulmonary environmental effects on the resident AM allowing for exploitation of the AM as a susceptible and permissive niche for infection.;In the context of C. neoformans infection, we found that only a restricted population of C. neoformans replicated in AMs. The majority of C. neoformans that replicated in vivo did so extracellularly and the extent of extracellular replication exceeded intracellular replication of the yeast. In fact, the majority of intracellular fungal load in AMs at 48 hours post-infection was attributable to the uptake of extracellular C. neoformans from 24 to 48 hours post-infection. Thus, unlike C. burnetii, C. neoformans does not appear to exploit the pulmonary environmental effects on the resident AM during establishment of infection.;Through the identification of the AM as a susceptible and permissive niche for C. burnetii infection and the finding that C. neoformans replicates primarily extracellularly during early pulmonary infection, we have both filled a deficiency in the previous knowledge base and set the stage for future studies into the induction of subsequent adaptive immune responses during these varied infections.
机译：在控制伴随的组织损伤的同时，肺必须对病原体发起有效的免疫反应。这种协调的中心是肺环境对局部肺泡巨噬细胞（AM）产生的免疫调节作用。此外，已知细胞内病原体可利用宿主免疫系统。由于这个原因，我们假设驻留的AM将包含能够被细胞内病原体利用的脆弱细胞群。为了检验这一假设，我们研究了AM在专性细胞内细菌柯氏杆菌或兼性细胞内真菌新隐球菌肺部感染中的作用；我们证明了[1]驻地AM确实是最容易感染的细胞类型。伯氏梭菌感染。这些常驻AM最多可感染十二天，可作为支持细菌生存的小生境。另外，受感染的AM的一个子集响应于感染经历特征性的表型改变，导致表面整联蛋白CD11b的表达增加和表面整联蛋白CD11c的持续表达。我们的结论是，伯氏梭状芽胞杆菌能够利用对居民AM的肺部环境影响，从而允许将AM用作感染的易感和容许位。；在新孢梭菌感染的情况下，我们发现只有有限的种群在AM中复制的新形成梭状芽胞杆菌。在体内复制的大多数新孢梭菌在细胞外复制，并且细胞外复制的程度超过了酵母的细胞内复制。实际上，感染后48小时AM中大多数细胞内真菌负荷是由于感染后24至48小时摄取胞外新孢梭菌。因此，与伯氏梭状芽孢杆菌不同，新福寿螺菌似乎在感染建立期间未利用其对居民AM的肺环境影响。;通过将AM鉴定为伯氏梭状芽孢杆菌感染的易感和允许生态位，并发现C. neoformans主要在早期肺部感染期间主要在细胞外复制，我们都填补了以前的知识库中的不足，并为以后研究在这些不同感染期间诱导随后的适应性免疫应答奠定了基础。

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  • 作者

    Calverley, Matthew David.;

  • 作者单位

    Montana State University.;

  • 授予单位 Montana State University.;
  • 学科 Health Sciences Immunology.
  • 学位 Ph.D.
  • 年度 2013
  • 页码 141 p.
  • 总页数 141
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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