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1
Escherichia coli-induced activation of neutrophil NADPH-oxidase: lipopolysaccharide and formylated peptides act synergistically to induce release of reactive oxygen metabolites.大肠杆菌诱导的中性粒细胞NADPH氧化酶激活:脂多糖和甲酰化肽协同作用诱导活性氧代谢产物的释放。
Infect Immun. 1995 Dec;63(12):4606-12. doi: 10.1128/iai.63.12.4606-4612.1995.
2
NADPH-oxidase activation in murine neutrophils via formyl peptide receptors.通过甲酰肽受体激活小鼠中性粒细胞中的NADPH氧化酶。
Exp Cell Res. 2003 Jan 15;282(2):70-7. doi: 10.1016/s0014-4827(02)00010-1.
3
Neutrophil control of formylmethionyl-leucyl-phenylalanine induced mobilization of secretory vesicles and NADPH-oxidase activation: effect of an association of the ligand-receptor complex to the cytoskeleton.中性粒细胞对甲酰甲硫氨酰-亮氨酰-苯丙氨酸诱导的分泌囊泡动员和NADPH氧化酶激活的控制:配体-受体复合物与细胞骨架结合的作用
Biochim Biophys Acta. 1994 Oct 20;1224(1):43-50. doi: 10.1016/0167-4889(94)90111-2.
4
Chemoattractant-induced NADPH oxidase activity in human monocytes is terminated without any association of receptor-ligand complex to cytoskeleton.趋化因子诱导的人类单核细胞中的NADPH氧化酶活性被终止,且受体-配体复合物与细胞骨架无任何关联。
Inflammation. 1995 Apr;19(2):179-91. doi: 10.1007/BF01534460.
5
Regulation of neutrophil NADPH oxidase activation in a cell-free system by guanine nucleotides and fluoride. Evidence for participation of a pertussis and cholera toxin-insensitive G protein.鸟嘌呤核苷酸和氟化物在无细胞体系中对中性粒细胞NADPH氧化酶激活的调节。百日咳毒素和霍乱毒素不敏感的G蛋白参与的证据。
J Biol Chem. 1987 Feb 5;262(4):1685-90.
6
Desensitization of formyl peptide receptors is abolished in calcium ionophore-primed neutrophils: an association of the ligand-receptor complex to the cytoskeleton is not required for a rapid termination of the NADPH-oxidase response.钙离子载体预处理的中性粒细胞中,甲酰肽受体脱敏作用消失:NADPH氧化酶反应的快速终止并不需要配体-受体复合物与细胞骨架结合。
J Immunol. 1998 Mar 1;160(5):2463-8.
7
Histamine inhibits neutrophil NADPH oxidase activity triggered by the lipoxin A4 receptor-specific peptide agonist Trp-Lys-Tyr-Met-Val-Met.组胺可抑制由脂氧素A4受体特异性肽激动剂色氨酸-赖氨酸-酪氨酸-甲硫氨酸-缬氨酸-甲硫氨酸触发的中性粒细胞NADPH氧化酶活性。
Scand J Immunol. 2003 Sep;58(3):321-6. doi: 10.1046/j.1365-3083.2003.01301.x.
8
The N-formylpeptide receptor (FPR) and a second G(i)-coupled receptor mediate fMet-Leu-Phe-stimulated activation of NADPH oxidase in murine neutrophils.N-甲酰肽受体(FPR)和第二种G(i)偶联受体介导甲酰甲硫氨酰-亮氨酰-苯丙氨酸(fMet-Leu-Phe)刺激的小鼠中性粒细胞中NADPH氧化酶的激活。
Cell Immunol. 2002 Jul-Aug;218(1-2):7-12. doi: 10.1016/s0008-8749(02)00564-6.
9
Lipopolysaccharide-induced gelatinase granule mobilization primes neutrophils for activation by galectin-3 and formylmethionyl-Leu-Phe.脂多糖诱导的明胶酶颗粒动员使中性粒细胞对半乳糖凝集素-3和甲酰甲硫氨酰-亮氨酰-苯丙氨酸激活产生预适应。
Infect Immun. 2001 Feb;69(2):832-7. doi: 10.1128/IAI.69.2.832-837.2001.
10
Desensitization of the fMLP-induced NADPH-oxidase response in human neutrophils is lacking in okadaic acid-treated cells.在经冈田酸处理的细胞中,人中性粒细胞中fMLP诱导的NADPH氧化酶反应缺乏脱敏现象。
J Leukoc Biol. 1997 Jun;61(6):753-8. doi: 10.1002/jlb.61.6.753.

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Aged gut microbiota contribute to different changes in antioxidant defense in the heart and liver after transfer to germ-free mice.老年肠道微生物群在转移到无菌小鼠后导致心脏和肝脏抗氧化防御的不同变化。
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Front Pharmacol. 2022 Jan 4;12:814113. doi: 10.3389/fphar.2021.814113. eCollection 2021.
4
The Prolyl Isomerase Pin1 Controls Lipopolysaccharide-Induced Priming of NADPH Oxidase in Human Neutrophils.脯氨酰异构酶 Pin1 控制人中性粒细胞中脂多糖诱导的 NADPH 氧化酶的激活。
Front Immunol. 2019 Nov 1;10:2567. doi: 10.3389/fimmu.2019.02567. eCollection 2019.
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Cellular and Site-Specific Mitochondrial Characterization of Vital Human Amniotic Membrane.重要人羊膜的细胞和部位特异性线粒体特征分析。
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The role of formylated peptides and formyl peptide receptor 1 in governing neutrophil function during acute inflammation.甲酰化肽和甲酰肽受体1在急性炎症期间调控中性粒细胞功能中的作用。
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Role of formyl peptide receptor-like 1 (FPRL1/FPR2) in mononuclear phagocyte responses in Alzheimer disease.甲酰肽受体样1(FPRL1/FPR2)在阿尔茨海默病单核吞噬细胞反应中的作用
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Uropathogenic Escherichia coli triggers oxygen-dependent apoptosis in human neutrophils through the cooperative effect of type 1 fimbriae and lipopolysaccharide.尿路致病性大肠杆菌通过1型菌毛和脂多糖的协同作用触发人中性粒细胞的氧依赖性凋亡。
Infect Immun. 2004 Aug;72(8):4570-8. doi: 10.1128/IAI.72.8.4570-4578.2004.
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Subinhibitory concentrations of the deformylase inhibitor actinonin increase bacterial release of neutrophil-activating peptides: a new approach to antimicrobial chemotherapy.去甲酰化酶抑制剂放线菌素的亚抑制浓度可增加细菌释放中性粒细胞激活肽:抗菌化疗的新方法。
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10
Human granulocytic ehrlichiosis agent inhibits superoxide anion generation by human neutrophils.人粒细胞埃立克体抑制人中性粒细胞产生超氧阴离子。
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本文引用的文献

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Control of exocytosis in early neutrophil activation.早期中性粒细胞激活过程中胞吐作用的调控
J Immunol. 1993 Feb 15;150(4):1535-43.
2
Subcellular localization and dynamics of Mac-1 (alpha m beta 2) in human neutrophils.人类中性粒细胞中Mac-1(αmβ2)的亚细胞定位与动力学
J Clin Invest. 1993 Sep;92(3):1467-76. doi: 10.1172/JCI116724.
3
Subcellular localization and translocation of the receptor for N-formylmethionyl-leucyl-phenylalanine in human neutrophils.人中性粒细胞中N-甲酰甲硫氨酰-亮氨酰-苯丙氨酸受体的亚细胞定位与转运
Biochem J. 1994 Apr 15;299 ( Pt 2)(Pt 2):473-9. doi: 10.1042/bj2990473.
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Secretory vesicles are the intracellular reservoir of complement receptor 1 in human neutrophils.分泌囊泡是人类中性粒细胞中补体受体1的细胞内储存库。
J Immunol. 1994 Jul 15;153(2):804-10.
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Quartz selectively down-regulates CR1 on activated human granulocytes.
J Leukoc Biol. 1993 Jan;53(1):99-103. doi: 10.1002/jlb.53.1.99.
6
Mobilization of granules and secretory vesicles during in vivo exudation of human neutrophils.人中性粒细胞体内渗出过程中颗粒和分泌小泡的动员
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Phagocyte strategy vs. microbial tactics.吞噬细胞策略与微生物战术
Rev Infect Dis. 1980 Sep-Oct;2(5):817-38. doi: 10.1093/clinids/2.5.817.
8
The ultrastructural localization of human neutrophil alkaline phosphatase in normal individuals during pregnancy and in patients with chronic granulocytic leukaemia.正常妊娠个体及慢性粒细胞白血病患者中性粒细胞碱性磷酸酶的超微结构定位
Histochem J. 1981 Jan;13(1):31-43. doi: 10.1007/BF01005837.
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Purification and characterization of neutrophil chemotactic factors of Streptococcus sanguis.血链球菌中性粒细胞趋化因子的纯化与特性分析
Biochim Biophys Acta. 1983 Jul 29;758(2):181-6. doi: 10.1016/0304-4165(83)90300-8.
10
Purification and identification of formyl-methionyl-leucyl-phenylalanine as the major peptide neutrophil chemotactic factor produced by Escherichia coli.将甲酰甲硫氨酰亮氨酰苯丙氨酸纯化并鉴定为大肠杆菌产生的主要肽中性粒细胞趋化因子。
J Biol Chem. 1984 May 10;259(9):5430-9.

大肠杆菌诱导的中性粒细胞NADPH氧化酶激活:脂多糖和甲酰化肽协同作用诱导活性氧代谢产物的释放。

Escherichia coli-induced activation of neutrophil NADPH-oxidase: lipopolysaccharide and formylated peptides act synergistically to induce release of reactive oxygen metabolites.

作者信息

Karlsson A, Markfjäll M, Strömberg N, Dahlgren C

机构信息

Department of Medical Microbiology and Immunology, Faculty of Odontology, University of Göteborg, Sweden.

出版信息

Infect Immun. 1995 Dec;63(12):4606-12. doi: 10.1128/iai.63.12.4606-4612.1995.

DOI:10.1128/iai.63.12.4606-4612.1995
PMID:7591113
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC173662/
Abstract

The prevailing view of neutrophil NADPH-oxidase activation during interaction with bacteria is that the production of toxic oxygen metabolites should be directed into the phagosome containing the engulfed prey. However, in this report we show that a common Escherichia coli strain, HB101, may induce a release of neutrophil oxygen metabolites to the extracellular milieu. This phenomenon is dependent on three factors: (i) the mobilization (upregulation) of neutrophil secretory vesicles prior to interaction with the bacteria, (ii) soluble bacterial factors binding to the formylmethionyl-leucyl-phenylalanine receptor and tentatively identified as formylated peptides, and (iii) a bacterium-associated priming factor identified as lipopolysaccharide.

摘要

关于中性粒细胞与细菌相互作用期间NADPH氧化酶激活的普遍观点是,有毒氧代谢产物的产生应导向含有被吞噬猎物的吞噬体。然而,在本报告中我们表明,一种常见的大肠杆菌菌株HB101可能会诱导中性粒细胞氧代谢产物释放到细胞外环境中。这种现象取决于三个因素:(i)中性粒细胞分泌囊泡在与细菌相互作用之前的动员(上调),(ii)与甲酰甲硫氨酰亮氨酰苯丙氨酸受体结合并初步鉴定为甲酰化肽的可溶性细菌因子,以及(iii)一种被鉴定为脂多糖的细菌相关启动因子。