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1
Inheritance of lipopolysaccharide-enhanced nonspecific resistance to infection and of susceptibility to endotoxic shock in lipopolysaccharide low-responder mice.脂多糖低反应小鼠中脂多糖增强的非特异性抗感染抵抗力及对内毒素休克易感性的遗传
Infect Immun. 1977 May;16(2):432-38. doi: 10.1128/iai.16.2.432-438.1977.
2
[Non-specific responses of C3H/He low responder mice to LPS and to TCA-extracted endotoxin].
Ann Immunol (Paris). 1977 Jan-Mar;128(1-2):67-9.
3
Failure of endotoxin to increase nonspecific resistance to infection of lipopolysaccharide low-responder mice.内毒素未能增强脂多糖低反应小鼠对感染的非特异性抵抗力。
Infect Immun. 1976 Mar;13(3):722-7. doi: 10.1128/iai.13.3.722-727.1976.
4
Transfer by bone marrow cells of increased natural resistance to Klebsiella pneumoniae induced by lipopolysaccharide in genetically deficient C3H/He mice.在基因缺陷的C3H/He小鼠中,通过骨髓细胞转移由脂多糖诱导产生的对肺炎克雷伯菌增强的天然抵抗力。
Infect Immun. 1979 Feb;23(2):232-8. doi: 10.1128/iai.23.2.232-238.1979.
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Lps(d)/Ran of endotoxin-resistant C3H/HeJ mice is defective in mediating lipopolysaccharide endotoxin responses.内毒素抗性C3H/HeJ小鼠的Lps(d)/Ran在介导脂多糖内毒素反应方面存在缺陷。
Proc Natl Acad Sci U S A. 1999 Sep 28;96(20):11543-8. doi: 10.1073/pnas.96.20.11543.
6
Mechanisms of endotoxin shock and endotoxin hypersensitivity.内毒素休克和内毒素超敏反应的机制。
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7
Genetical control of B-cell responses. IV. Inheritance of the unresponsiveness to lipopolysaccharides.B细胞应答的遗传控制。IV. 对脂多糖无反应性的遗传
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8
Genetic analysis of lymphocyte activation by lipopolysaccharide Endotoxin.脂多糖内毒素对淋巴细胞激活的遗传分析。
Infect Immun. 1976 Jun;13(6):1579-84. doi: 10.1128/iai.13.6.1579-1584.1976.
9
The response of recombinant inbred strains of mice to bacterial lipopolysaccharides.小鼠重组近交系对细菌脂多糖的反应。
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Role of B-lymphocytes in nonspecific resistance to Klebsiella pneumoniae infection of endotoxin-treated mice.
J Infect Dis. 1976 Dec;134(6):531-9. doi: 10.1093/infdis/134.6.531.

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Stage of primary infection with lymphocytic choriomeningitis virus determines predisposition or resistance of mice to secondary bacterial infections.淋巴细胞性脉络丛脑膜炎病毒原发性感染的阶段决定了小鼠对继发性细菌感染的易感性或抵抗力。
Med Microbiol Immunol. 2007 Jun;196(2):79-88. doi: 10.1007/s00430-006-0030-1. Epub 2006 Nov 29.
3
Beneficial or deleterious effects of a preexisting hypersensitivity to bacterial components on the course and outcome of infection.先前存在的对细菌成分的超敏反应对感染过程和结果的有益或有害影响。
Infect Immun. 2002 Oct;70(10):5596-603. doi: 10.1128/IAI.70.10.5596-5603.2002.
4
Enhancement of resistance to infections by endotoxin-induced serum factor from Mycobacterium bovis BCG-infected mice.卡介苗感染小鼠的内毒素诱导血清因子增强对感染的抵抗力
Infect Immun. 1980 Jun;28(3):654-9. doi: 10.1128/iai.28.3.654-659.1980.
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Susceptibility of inbred mouse strains to infection with Serpula (Treponema) hyodysenteriae.近交系小鼠品系对猪痢疾密螺旋体感染的易感性。
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6
Distribution of endotoxin (lipopolysaccharide) in the tissues of lipopolysaccharide-responsive and -unresponsive mice.脂多糖反应性和无反应性小鼠组织中内毒素(脂多糖)的分布
Infect Immun. 1978 Aug;21(2):448-57. doi: 10.1128/iai.21.2.448-457.1978.
7
Transfer by bone marrow cells of increased natural resistance to Klebsiella pneumoniae induced by lipopolysaccharide in genetically deficient C3H/He mice.在基因缺陷的C3H/He小鼠中,通过骨髓细胞转移由脂多糖诱导产生的对肺炎克雷伯菌增强的天然抵抗力。
Infect Immun. 1979 Feb;23(2):232-8. doi: 10.1128/iai.23.2.232-238.1979.

本文引用的文献

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High Susceptibility of Strain A Mice to Endotoxin and Endotoxin-Red Blood Cell Mixtures.A品系小鼠对内毒素及内毒素-红细胞混合物高度敏感。
J Bacteriol. 1965 Sep;90(3):696-703. doi: 10.1128/jb.90.3.696-703.1965.
2
[INCREASE IN RESISTANCE TO INFECTIONS FOLLOWING AN ENDOTOXIN INJECTION. DEMONSTRATION OF THE MECHANISM BY SULFONAMIDE ASSOCIATION].[内毒素注射后抗感染能力的增强。通过磺胺类药物联合使用对机制的证明]
C R Hebd Seances Acad Sci. 1965 Mar 1;260:2630-3.
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Characterization of a Cr51-labeled endotoxin and its identification in plasma and urine after parenteral administration.一种铬51标记的内毒素的特性及其在肠胃外给药后在血浆和尿液中的鉴定。
J Exp Med. 1963 Apr 1;117(4):561-71. doi: 10.1084/jem.117.4.561.
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[Study of the tolerance of adrenalectomized mice using an endotoxin labeled with Cr-51].[使用51铬标记的内毒素对肾上腺切除小鼠耐受性的研究]
Ann Inst Pasteur (Paris). 1961 Aug;101:170-7.
5
Reversible changes in the susceptibility of mice to bacterial infections. I. Changes brought about by injection of pertussis vaccine or of bacterial endotoxins.小鼠对细菌感染易感性的可逆变化。I. 注射百日咳疫苗或细菌内毒素引起的变化。
J Exp Med. 1956 Jul 1;104(1):53-65. doi: 10.1084/jem.104.1.53.
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Studies on the O antigen of Salmonella typhosa. V. Enhancement of antibody response to protein antigens by the purified lipopolysaccharide.伤寒沙门氏菌O抗原的研究。V. 纯化脂多糖增强对蛋白质抗原的抗体反应。
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Stimulation of natural immunity to Escherichia coli infection: observations on mice.对大肠杆菌感染天然免疫的刺激:对小鼠的观察
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[Study of opsonins in mice after endotoxin augmentation of their resistance to infection].[内毒素增强小鼠抗感染能力后调理素的研究]
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9
The primary immune response in mice. I. The enhancement and suppression of hemolysin production by a bacterial endotoxin.小鼠的初次免疫反应。I. 细菌内毒素对溶血素产生的增强和抑制作用。
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10
Localization and fate of 51-Cr-labeled somatic antigens of smooth and rough Salmonellae.光滑型和粗糙型沙门氏菌51铬标记体细胞抗原的定位与归宿
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脂多糖低反应小鼠中脂多糖增强的非特异性抗感染抵抗力及对内毒素休克易感性的遗传

Inheritance of lipopolysaccharide-enhanced nonspecific resistance to infection and of susceptibility to endotoxic shock in lipopolysaccharide low-responder mice.

作者信息

Parant M, Parant F, Chedid L

出版信息

Infect Immun. 1977 May;16(2):432-38. doi: 10.1128/iai.16.2.432-438.1977.

DOI:10.1128/iai.16.2.432-438.1977
PMID:863509
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC420968/
Abstract

In a previous study, we demonstrated that lipopolysaccharide (LPS) and other bacterial immunostimulants, in contrast to their activity in a closely related high-responder subline, failed to elicit nonspecific resistance in LPS low-responder mice against Klebsiella pneumoniae infection. To investigate the type of inheritance controlling the LPS-induced nonspecific resistance to infection, the present study was performed in low- and high-responder C3H sublines and in F1 and F2 hybrids. In addition, F1 mice were backcrossed to each parental type. Inheritance of susceptibility to endotoxin was also tested in both sublines and their hybrids and backcross progeny. For these latter assays, mice were previously adrenalectomized because removal of this gland considerably enhances their sensitivity. Our present findings are consistent with the hypothesis that LPS enhances nonspecific resistance to infection and that susceptibility to endotoxin shock in the absence of corticoids may be determined by a single autosomal dominant gene.

摘要

在先前的一项研究中,我们证明,与脂多糖(LPS)及其他细菌免疫刺激剂在密切相关的高反应性子系中的活性相反,它们无法在LPS低反应性小鼠中引发对肺炎克雷伯菌感染的非特异性抵抗力。为了研究控制LPS诱导的抗感染非特异性抵抗力的遗传类型,本研究在低反应性和高反应性C3H子系以及F1和F2杂种中进行。此外,F1小鼠与每种亲本类型进行回交。还在两个子系及其杂种和回交后代中测试了对内毒素易感性的遗传。对于后一种试验,小鼠事先进行了肾上腺切除术,因为切除该腺体可大大提高它们的敏感性。我们目前的研究结果与以下假设一致,即LPS增强了对感染的非特异性抵抗力,并且在没有皮质激素的情况下对内毒素休克的易感性可能由单个常染色体显性基因决定。