• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

微生物、巨噬细胞与一氧化氮

Of microbes, macrophages and nitric oxide.

作者信息

Bogdan C

机构信息

Institute of Clinical Microbiology and Immunology, University of Erlangen, Germany.

出版信息

Behring Inst Mitt. 1997 Mar(99):58-72.

PMID:9303203
Abstract

One of the most prominent functions of nitric oxide (NO) is its participation in antimicrobial and antiviral defense. This paper summarizes the evidence for this function and compiles the infectious agents which are currently thought to be controlled via high out-put generation of NO as it occurs in activated macrophages and other cells expressing the inducible isoform of NO-synthase (iNOS, NOS-2). Several less appreciated forms of interaction between NO and microbes will also be reviewed, including the role of NO as an immunosuppressive or tissue-destructive molecule during the course of infections, the regulation of microbial antioxidant systems by host cell-derived NO, the contribution of NO to parasite stage conversion, the induction or suppression of macrophage iNOS by microbial products, and the existence of endogenous NO synthase pathways in certain bacteria and parasites.

摘要

一氧化氮(NO)最显著的功能之一是其参与抗菌和抗病毒防御。本文总结了这一功能的证据,并汇编了目前认为通过在活化巨噬细胞和其他表达诱导型一氧化氮合酶(iNOS,NOS-2)同工型的细胞中发生的高产量NO生成来控制的感染因子。还将综述NO与微生物之间几种较少被认识到的相互作用形式,包括NO在感染过程中作为免疫抑制或组织破坏分子的作用、宿主细胞衍生的NO对微生物抗氧化系统的调节、NO对寄生虫阶段转换的贡献、微生物产物对巨噬细胞iNOS的诱导或抑制,以及某些细菌和寄生虫中内源性一氧化氮合酶途径的存在。

相似文献

1
Of microbes, macrophages and nitric oxide.微生物、巨噬细胞与一氧化氮
Behring Inst Mitt. 1997 Mar(99):58-72.
2
Effects of ethanol on neutrophil recruitment and lung host defense in nitric oxide synthase I and nitric oxide synthase II knockout mice.乙醇对一氧化氮合酶I和一氧化氮合酶II基因敲除小鼠中性粒细胞募集及肺部宿主防御的影响。
Alcohol Clin Exp Res. 1999 Sep;23(9):1435-45.
3
[The antimicrobial activity of nitric oxide and its role in the infectious process].[一氧化氮的抗菌活性及其在感染过程中的作用]
Zh Mikrobiol Epidemiol Immunobiol. 1999 Sep-Oct(5):61-7.
4
Nitric oxide and the immune response.一氧化氮与免疫反应。
Nat Immunol. 2001 Oct;2(10):907-16. doi: 10.1038/ni1001-907.
5
Propofol reduces nitric oxide biosynthesis in lipopolysaccharide-activated macrophages by downregulating the expression of inducible nitric oxide synthase.丙泊酚通过下调诱导型一氧化氮合酶的表达来降低脂多糖激活的巨噬细胞中一氧化氮的生物合成。
Arch Toxicol. 2003 Jul;77(7):418-23. doi: 10.1007/s00204-003-0453-z. Epub 2003 Mar 12.
6
Involvement of protein kinase C and not of NF kappa B in the modulation of macrophage nitric oxide synthase by tumor-derived phosphatidyl serine.蛋白激酶C而非核因子κB参与肿瘤衍生磷脂酰丝氨酸对巨噬细胞一氧化氮合酶的调节。
Int J Oncol. 2008 Mar;32(3):713-21.
7
[Immune mechanisms of antiviral, bacterial and parasitic protection].[抗病毒、抗细菌和抗寄生虫保护的免疫机制]
Rev Ig Bacteriol Virusol Parazitol Epidemiol Pneumoftiziol Bacteriol Virusol Parazitol Epidemiol. 1988 Jan-Mar;33(1):15-28.
8
Vasoactive intestinal peptide and pituitary adenylate cyclase-activating polypeptide prevent inducible nitric oxide synthase transcription in macrophages by inhibiting NF-kappa B and IFN regulatory factor 1 activation.血管活性肠肽和垂体腺苷酸环化酶激活多肽通过抑制核因子κB和干扰素调节因子1的激活来阻止巨噬细胞中诱导型一氧化氮合酶的转录。
J Immunol. 1999 Apr 15;162(8):4685-96.
9
[The patient with impaired defense against infections. Types of defect and spectrum of infectious diseases].[抗感染防御功能受损的患者。缺陷类型及传染病谱]
Tidsskr Nor Laegeforen. 1983 Jan 30;103(3):213-9.
10
The role of nitric oxide in bladder urothelial injury after bladder outlet obstruction.一氧化氮在膀胱出口梗阻后膀胱尿路上皮损伤中的作用。
BJU Int. 2004 Aug;94(3):392-9. doi: 10.1111/j.1464-410X.2004.04968.x.

引用本文的文献

1
Nitric Oxide Inhibition of Rickettsia rickettsii.抑制立氏立克次体的一氧化氮。
Infect Immun. 2021 Nov 16;89(12):e0037121. doi: 10.1128/IAI.00371-21. Epub 2021 Sep 7.
2
The TLR4-NOS1-AP1 signaling axis regulates macrophage polarization.TLR4-NOS1-AP1 信号轴调节巨噬细胞极化。
Inflamm Res. 2017 Apr;66(4):323-334. doi: 10.1007/s00011-016-1017-z. Epub 2016 Dec 24.
3
Arginine Metabolism in Bacterial Pathogenesis and Cancer Therapy.细菌致病机制与癌症治疗中的精氨酸代谢
Int J Mol Sci. 2016 Mar 11;17(3):363. doi: 10.3390/ijms17030363.
4
Entry and elimination of marine mammal Brucella spp. by hooded seal (Cystophora cristata) alveolar macrophages in vitro.体外实验中海豹(Cystophora cristata)肺泡巨噬细胞对海洋哺乳动物布鲁氏菌属的吞噬和清除作用。
PLoS One. 2013 Jul 25;8(7):e70186. doi: 10.1371/journal.pone.0070186. Print 2013.
5
From inflammation to wound healing: using a simple model to understand the functional versatility of murine macrophages.从炎症到伤口愈合:利用简单模型了解小鼠巨噬细胞的功能多样性。
Bull Math Biol. 2011 Nov;73(11):2575-604. doi: 10.1007/s11538-011-9637-5. Epub 2011 Feb 23.
6
Liver injury and abscess formation in secondary murine peritonitis.继发性腹膜炎小鼠的肝损伤和脓肿形成。
Inflamm Res. 2011 Apr;60(4):337-45. doi: 10.1007/s00011-010-0273-6. Epub 2010 Oct 26.
7
Augmented inducible nitric oxide synthase expression and increased NO production reduce sepsis-induced lung injury and mortality in myeloperoxidase-null mice.髓过氧化物酶缺陷小鼠中,增强的诱导型一氧化氮合酶表达及增加的一氧化氮生成可减轻脓毒症诱导的肺损伤并降低死亡率。
Am J Physiol Lung Cell Mol Physiol. 2008 Jul;295(1):L96-103. doi: 10.1152/ajplung.00450.2007. Epub 2008 Apr 18.
8
Peritoneal lavage cells of Indonesian thin-tail sheep mediate antibody-dependent superoxide radical cytotoxicity in vitro against newly excysted juvenile Fasciola gigantica but not juvenile Fasciola hepatica.印度尼西亚细尾绵羊的腹腔灌洗细胞在体外介导抗体依赖性超氧自由基细胞毒性作用,对抗新脱囊的巨片形吸虫幼虫,但对肝片形吸虫幼虫无此作用。
Infect Immun. 2007 Apr;75(4):1954-63. doi: 10.1128/IAI.01034-06. Epub 2007 Jan 8.
9
Comparison of gamma interferon-mediated antichlamydial defense mechanisms in human and mouse cells.γ干扰素介导的人类和小鼠细胞抗衣原体防御机制的比较。
Infect Immun. 2006 Jan;74(1):225-38. doi: 10.1128/IAI.74.1.225-238.2006.
10
Thioredoxin peroxidase secreted by Fasciola hepatica induces the alternative activation of macrophages.肝片吸虫分泌的硫氧还蛋白过氧化物酶可诱导巨噬细胞的替代性活化。
Infect Immun. 2005 Jan;73(1):166-73. doi: 10.1128/IAI.73.1.166-173.2005.