...
首页> 外文期刊>Immunology: An Official Journal of the British Society for Immunology >Mast cells are activated by Staphylococcus aureus in vitro but do not influence the outcome of intraperitoneal S. aureus infection in vivo.
【24h】

Mast cells are activated by Staphylococcus aureus in vitro but do not influence the outcome of intraperitoneal S. aureus infection in vivo.

机译:肥大细胞在体外被金黄色葡萄球菌激活,但在体内不影响腹膜内金黄色葡萄球菌感染的结果。

获取原文
获取原文并翻译 | 示例

摘要

Staphylococcus aureus is a major pathogen that can cause a broad spectrum of serious infections including skin infections, pneumonia and sepsis. Peritoneal mast cells have been implicated in the host response towards various bacterial insults and to provide mechanistic insight into the role of mast cells in intraperitoneal bacterial infection we here studied the global effects of S. aureus on mast cell gene expression. After co-culture of peritoneal mast cells with live S. aureus we found by gene array analysis that they up-regulate a number of genes. Many of these corresponded to pro-inflammatory cytokines, including interleukin-3, interleukin-13 and tumour necrosis factor-α. The cytokine induction in response to S. aureus was confirmed by ELISA. To study the role of peritoneal mast cells during in vivo infection with S. aureus we used newly developed Mcpt5-Cre(+) × R-DTA mice in which mast cell deficiency is independent of c-Kit. This is in contrast to previous studies in which an impact of mast cells on bacterial infection has been proposed based on the use of mice whose mast cell deficiency is a consequence of defective c-Kit signalling. Staphylococcus aureus was injected intraperitoneally into mast-cell-deficient Mcpt5-Cre(+) × R-DTA mice using littermate mast-cell-sufficient mice as controls. We did not observe any difference between mast-cell-deficient and control mice with regard to weight loss, bacterial clearance, inflammation or cytokine production. We conclude that, despite peritoneal mast cells being activated by S. aureus in vitro, they do not influence the in vivo manifestations of intraperitoneal S. aureus infection.
机译:金黄色葡萄球菌是一种主要病原体,可引起多种严重感染,包括皮肤感染,肺炎和败血症。腹膜肥大细胞已牵连到宿主对各种细菌侵害的反应中,并且为了提供有关肥大细胞在腹膜内细菌感染中作用的机制的见解,我们在这里研究了金黄色葡萄球菌对肥大细胞基因表达的整体影响。腹膜肥大细胞与活金黄色葡萄球菌共培养后,我们通过基因阵列分析发现它们上调了许多基因。这些中的许多对应于促炎细胞因子,包括白介素-3,白介素13和肿瘤坏死因子-α。通过ELISA确认了响应金黄色葡萄球菌的细胞因子诱导。为了研究金黄色葡萄球菌在体内感染期间腹膜肥大细胞的作用,我们使用了新开发的Mcpt5-Cre(+)×R-DTA小鼠,其中肥大细胞的缺乏独立于c-Kit。这与先前的研究相反,在先前的研究中,已经基于肥大细胞缺乏是c-Kit信号传导缺陷的结果的小鼠的使用,提出了肥大细胞对细菌感染的影响。将金黄色葡萄球菌腹膜内注射到肥大细胞缺乏的Mcpt5-Cre(+)×R-DTA小鼠中,使用同窝出生的肥大细胞的小鼠作为对照。在体重减轻,细菌清除,炎症或细胞因子产生方面,我们未观察到肥大细胞缺陷小鼠和对照小鼠之间的任何差异。我们得出结论,尽管腹膜肥大细胞在体外被金黄色葡萄球菌激活,但它们不影响腹膜内金黄色葡萄球菌感染的体内表现。

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