• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Infection and immunity >Differential Innate Immune Cell Activation and Proinflammatory Response in Anaplasma phagocytophilum Infection
【24h】

Differential Innate Immune Cell Activation and Proinflammatory Response in Anaplasma phagocytophilum Infection

机译：差异性先天免疫细胞活化和炎性浆细胞感染的促炎反应

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Human granulocytic anaplasmosis (HGA) is caused by the obligate intracellular bacterium Anaplasma phagocytophilum. The critical role of gamma interferon (IFN-γ) for induction of severe inflammatory histopathology, even in the absence of a significant bacterial load, was previously demonstrated in a murine model of HGA. We hypothesized that NK, NKT, and possibly CD8+ cytotoxic T cells participate in the development of histopathologic lesions with A. phagocytophilum infection. Mice were mock infected or infected with low- or high-passage A. phagocytophilum and assayed for hepatic histopathology and splenocyte immunophenotype during the first 21 days after infection. Compared to high-passage A. phagocytophilum-infected mice, low-passage A. phagocytophilum-infected mice had more severe hepatic lesions and increased apoptosis. The hepatic histopathology severity in low-passage A. phagocytophilum-infected mice peaked on day 2 at the time of peak plasma IFN-γ levels and gradually decreased through day 21. Low-passage A. phagocytophilum-infected mice also showed significantly increased levels of lymphocyte NK1.1/FasL expression on days 4 to 7 corresponding to early, severe hepatic inflammation, whereas the levels of NKT cells were substantially lower on day 4, suggesting that there was NKT cell involvement. This result supports the concept that NK1.1+ cells, including NK and NKT cells, are major components in the early pathogenesis of A. phagocytophilum infection.
机译：人类粒细胞性厌食症（HGA）是由专性细胞内细菌噬菌体嗜热菌引起的。先前已经在HGA的鼠模型中证明了即使在没有显着细菌负荷的情况下，γ干扰素（IFN-γ）在诱导严重炎性组织病理学中的关键作用。我们假设NK，NKT以及可能的CD8 + 细胞毒性T细胞参与了 A的组织病理学病变的发展。吞噬细胞感染。小鼠被模拟​​感染或被低或高通量的 A感染。并在感染后的头21天进行肝组织病理学检查和脾细胞免疫表型分析。与高通量 A相比。吞噬噬菌体感染的小鼠，低传代 A。吞噬吞噬细胞的小鼠肝脏病变更严重，细胞凋亡增加。低通量 A的肝组织病理学严重程度。感染吞噬细胞的小鼠在血浆IFN-γ水平达到峰值时在第2天达到峰值，并在第21天逐渐降低。感染了吞噬细胞的小鼠在第4至第7天还显示出明显升高的淋巴细胞NK1.1 / FasL表达水平，这与早期，严重的肝炎相对应，而在第4天，NKT细胞的水平则明显降低。涉及NKT细胞。该结果支持这样的概念，即NK1.1 + 细胞，包括NK和NKT细胞，是 A早期发病机理的主要组成部分。吞噬细胞感染。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号