• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Infection and immunity >Susceptibility of Germfree Phagocyte Oxidase- and Nitric Oxide Synthase 2-Deficient Mice, Defective in the Production of Reactive Metabolites of Both Oxygen and Nitrogen, to Mucosal and Systemic Candidiasis of Endogenous Origin
【24h】

Susceptibility of Germfree Phagocyte Oxidase- and Nitric Oxide Synthase 2-Deficient Mice, Defective in the Production of Reactive Metabolites of Both Oxygen and Nitrogen, to Mucosal and Systemic Candidiasis of Endogenous Origin

机译：生殖器官的粘膜和全身念珠菌病易受感染的无胚吞噬细胞氧化酶和一氧化氮合酶2缺陷小鼠的氧和氮反应性代谢产物的产生

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

摘要

Mice deficient for phagocyte oxidase (Phox) and nitric oxide synthase 2 (NOS2) (gp91phox?/?/NOS2?/?), defective in the production of both reactive oxygen intermediates (ROI) and reactive nitrogen intermediates (RNI), were used to investigate the role of phagocytic cells during mucosal and systemic candidiasis of endogenous origin. The alimentary tracts of germfree mice were colonized with Candida albicans wild type or each of two hyphal signaling-defective mutants (efg1/efg1 and efg1/efg1 cph1/cph1). All Candida-colonized gp91phox?/?/NOS2?/? mice were moribund within 12 to 15 days after oral inoculation. C. albicans wild-type and mutant strains colonized the alimentary tracts equally well and were able to translocate, most likely via Peyer's patches and mesenteric lymph nodes, to the internal organs and trigger the formation of abscesses; however, the wild-type and mutant strains did not survive in the abscessed murine tissues. Surprisingly, there was no significant difference in the ability of peritoneal exudate cells from gp91phox?/?/NOS2?/?, NOS2?/?, gp91phox?/?, or immunocompetent C57BL/6 mice to kill C. albicans in vitro. This suggests that anti-Candida factors other than ROI and RNI can control the growth of C. albicans and that gp91phox?/?/NOS2?/? mice die due to the inability of the host to control its inflammatory response to Candida. Correspondingly, reverse transcription-PCR analysis showed increased expression of the cytokines gamma interferon, tumor necrosis factor alpha, and the chemokines MIP-2 and KC at the site of infection, while interleukin-15 expression remained relatively unchanged between germfree and infected tissues. These studies indicate that defects in ROI and RNI enabled C. albicans to translocate and disseminate to the internal organs, resulting in an uncontrolled immune response, severe pathology, and death; however, ROI and RNI were not required for the killing of phagocytized C. albicans, indicating that other anti-Candida factors either compensate or are sufficient for the killing of phagocytized Candida.
机译：缺乏吞噬细胞氧化酶（Phox）和一氧化氮合酶2（NOS2）（gp91 phox？/？ / NOS2 ？/？）的小鼠，这两种小鼠均缺乏反应性氧气中间体（ROI）和活性氮中间体（RNI）用于研究吞噬细胞在内源性黏膜和全身念珠菌病中的作用。无菌小鼠的消化道定植于白色念珠菌野生型或两个菌丝信号缺陷的突变体（ efg1 / efg1 和 efg1 / efg1 cph1 / cph1 ）。口服接种后12到15天内，所有 Candida 克隆的gp91 phox？/？ / NOS2 ？/？sup>小鼠都垂死了。 C。白色念珠菌野生型和突变型菌株在消化道中的繁殖能力相同，并很可能通过派伊尔氏淋巴结和肠系膜淋巴结转移到内部器官，并引发脓肿。然而，野生型和突变株不能在脓肿的鼠组织中存活。令人惊讶的是，来自gp91 phox？/？ / NOS2 ？/？，NOS2 ？/？，gp91 phox？/？或具有免疫功能的C57BL / 6小鼠杀死 C。白色念珠菌这表明除ROI和RNI以外的抗 -Candida 因子也可以控制 C的生长。白色念珠菌和gp91 phox？/？ / NOS2 ？/？小鼠死于宿主无法控制其对 Candida的炎症反应。相应地，逆转录-PCR分析显示感染部位的细胞因子γ干扰素，肿瘤坏死因子α和趋化因子MIP-2和KC的表达增加，而白细胞介素15的表达在无菌组织和感染组织之间保持相对不变。这些研究表明，ROI和RNI的缺陷使 C成为可能。白色念珠易位并传播到内部器官，导致免疫反应失控，严重的病理状况和死亡;但是，吞噬吞噬的 C并不需要ROI和RNI。白色念珠菌，表明其他抗 Candida 因子补偿或足以杀死被吞噬的 Candida 。

著录项

相似文献

  • 外文文献
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