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首页> 外文期刊>Infection and immunity >Citrobacter koseri Brain Abscess in the Neonatal Rat: Survival and Replication within Human and Rat Macrophages
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Citrobacter koseri Brain Abscess in the Neonatal Rat: Survival and Replication within Human and Rat Macrophages

机译：新生大鼠中的科氏柠檬酸杆菌脑脓肿：在人类和大鼠巨噬细胞中的存活和复制

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A unique feature of Citrobacter koseri is the extremely high propensity to initiate brain abscesses during neonatal meningitis. Previous clinical reports and studies on infant rats have documented many Citrobacter-filled macrophages within the ventricles and brain abscesses. It has been hypothesized that intracellular survival and replication within macrophages may be a mechanism by which C. koseri subverts the host response and elicits chronic infection, resulting in brain abscess formation. In this study, we showed that C. koseri causes meningitis and brain abscesses in the neonatal rat model, and we utilized histology and magnetic resonance imaging technology to visualize brain abscess formation. Histology and electron microscopy (EM) revealed that macrophages (and not fibroblasts, astrocytes, oligodendrocytes, or neurons) were the primary target for long-term C. koseri infection. To better understand C. koseri pathogenesis, we have characterized the interactions of C. koseri with human macrophages. We found that C. koseri survives and replicates within macrophages in vitro and that uptake of C. koseri increases in the presence of human pooled serum in a dose-dependent manner. EM studies lend support to the hypothesis that C. koseri uses morphologically different methods of uptake to enter macrophages. FcγRI blocking experiments show that this receptor primarily facilitates the entry of opsonized C. koseri into macrophages. Further, confocal fluorescence microscopy demonstrates that C. koseri survives phagolysosomal fusion and that more than 90% of intracellular C. koseri organisms are colocalized within phagolysosomes. The ability of C. koseri to survive phagolysosome fusion and replicate within macrophages may contribute to the establishment of chronic central nervous system infection including brain abscesses.
机译：科氏柠檬酸杆菌的一个独特特征是在新生儿脑膜炎期间极易引发脑脓肿。先前有关婴儿大鼠的临床报告和研究已证明，脑室和脑脓肿中有许多充满柠檬酸的巨噬细胞。已经假设巨噬细胞内的细胞内存活和复制可能是 C的机制。 koseri 破坏宿主反应并引起慢性感染，导致脑脓肿形成。在这项研究中，我们显示了 C。 koseri 在新生大鼠模型中引起脑膜炎和脑脓肿，我们利用组织学和磁共振成像技术对脑脓肿的形成进行可视化。组织学和电子显微镜（EM）显示，巨噬细胞（而非成纤维细胞，星形胶质细胞，少突胶质细胞或神经元）是长期 C的主要靶标。 koseri 感染。为了更好地理解 C。 koseri 的发病机理，我们已经表征了 C的相互作用。人类巨噬细胞引起的koseri 。我们发现 C。 koseri 能够在体外巨噬细胞中存活并复制，并吸收 C。在人血中，koseri 呈剂量依赖性增加。 EM研究为 C的假设提供了支持。 koseri 使用形态学上不同的摄取方法进入巨噬细胞。 FcγRI阻断实验表明，该受体主要促进调理过的 C的进入。 koseri 变成巨噬细胞。此外，共聚焦荧光显微镜证明 C。 koseri 在吞噬体融合中幸存下来，并且细胞内 C的90％以上。 koseri 生物在吞噬溶酶体内共定位。 C的能力。噬菌体融合并在巨噬细胞内复制而生存的koseri 可能有助于建立包括脑脓肿在内的慢性中枢神经系统感染。

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