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本文引用的文献

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International collaborative study: evaluation of proposed International Reference Reagent of pertussis antiserum (mouse) 97/642.国际合作研究：对拟议的百日咳抗血清（小鼠）国际参考试剂97/642的评估。
Biologicals. 2001 Jun;29(2):137-48. doi: 10.1006/biol.2001.0288.
2
Serotype of Streptococcus pneumoniae capsular polysaccharide can modify the Th1/Th2 cytokine profile and IgG subclass response to pneumococal-CRM(197) conjugate vaccines in a murine model.在小鼠模型中，肺炎链球菌荚膜多糖的血清型可改变Th1/Th2细胞因子谱以及对肺炎球菌-CRM（197）结合疫苗的IgG亚类反应。
Vaccine. 2000 Dec 8;19(9-10):1159-66. doi: 10.1016/s0264-410x(00)00314-5.
3
Effect of pertussis toxin on the induction of nitric oxide synthesis in murine macrophages and on protection in vivo.百日咳毒素对小鼠巨噬细胞中一氧化氮合成诱导及体内保护作用的影响。
Vaccine. 2000 Apr 14;18(20):2110-9. doi: 10.1016/s0264-410x(99)00562-9.
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Effects of nitric oxide on the induction and differentiation of Th1 cells.一氧化氮对Th1细胞诱导和分化的影响。
Eur J Immunol. 1999 Aug;29(8):2498-505. doi: 10.1002/(SICI)1521-4141(199908)29:08<2498::AID-IMMU2498>3.0.CO;2-M.
5
An aerosol challenge model of Bordetella pertussis infection as a potential bioassay for acellular pertussis vaccines.百日咳博德特氏菌感染的气溶胶攻击模型作为无细胞百日咳疫苗的一种潜在生物测定法。
Vaccine. 1999 Feb 12;17(6):565-76. doi: 10.1016/s0264-410x(98)00235-7.
6
Nitric oxide regulates Th1 cell development through the inhibition of IL-12 synthesis by macrophages.一氧化氮通过抑制巨噬细胞合成白细胞介素-12来调节Th1细胞的发育。
Eur J Immunol. 1998 Dec;28(12):4062-70. doi: 10.1002/(SICI)1521-4141(199812)28:12<4062::AID-IMMU4062>3.0.CO;2-K.
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Nitric oxide induction in murine macrophages and spleen cells by whole-cell Bordetella pertussis vaccine.
Vaccine. 1998 Jan;16(1):16-23. doi: 10.1016/s0264-410x(97)00157-6.
8
Mice lacking inducible nitric-oxide synthase are more susceptible to herpes simplex virus infection despite enhanced Th1 cell responses.缺乏诱导型一氧化氮合酶的小鼠尽管Th1细胞反应增强，但对单纯疱疹病毒感染更易感。
J Gen Virol. 1998 Apr;79 ( Pt 4):825-30. doi: 10.1099/0022-1317-79-4-825.
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Septic arthritis following Staphylococcus aureus infection in mice lacking inducible nitric oxide synthase.
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10
In vitro and in vivo induction of nitric oxide by murine macrophages stimulated with Bordetella pertussis.百日咳博德特氏菌刺激的小鼠巨噬细胞在体外和体内诱导一氧化氮的产生
FEMS Immunol Med Microbiol. 1996 Feb;13(2):95-9. doi: 10.1016/0928-8244(95)00089-5.

一氧化氮在抵御百日咳博德特氏菌呼吸道感染中的作用研究。

Investigation of role of nitric oxide in protection from Bordetella pertussis respiratory challenge.

作者信息

Canthaboo C, Xing D, Wei X Q, Corbel M J

机构信息

Division of Bacteriology, National Institute for Biological Standards and Control, South Mimms, Potters Bar, Hertfordshire, EN6 3QG, United Kingdom.

出版信息

Infect Immun. 2002 Feb;70(2):679-84. doi: 10.1128/IAI.70.2.679-684.2002.

DOI:10.1128/IAI.70.2.679-684.2002
PMID:11796599
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC127720/
Abstract

The mechanism whereby whole-cell pertussis vaccines (WCV) confer protection against Bordetella pertussis is still not fully understood. We have previously reported that macrophage activation produced by vaccination with WCV is associated with induction of NO synthesis by macrophages in response to in vitro stimulation with B. pertussis antigens. To determine whether NO production is an effector of protection or simply a marker of activation, the susceptibility of inducible nitric oxide synthase (type II, iNOS) knockout mice to infection with B. pertussis was examined. We showed that iNOS knockout mice were more susceptible to B. pertussis respiratory challenge than wild-type mice. iNOS-deficient mice also developed a less effective protective response than wild-type mice after the same immunization with WCV. This suggests that NO plays an important role in effecting protection against B. pertussis challenge.

摘要

全细胞百日咳疫苗（WCV）提供针对百日咳博德特氏菌的保护作用的机制仍未完全了解。我们之前报道过，接种WCV所产生的巨噬细胞激活与巨噬细胞在体外受到百日咳博德特氏菌抗原刺激时诱导合成一氧化氮（NO）有关。为了确定NO的产生是保护作用的效应因子还是仅仅是激活的标志物，我们检测了诱导型一氧化氮合酶（II型，iNOS）基因敲除小鼠对百日咳博德特氏菌感染的易感性。我们发现，iNOS基因敲除小鼠比野生型小鼠对百日咳博德特氏菌的呼吸道攻击更易感。在用WCV进行相同免疫后，iNOS缺陷小鼠也比野生型小鼠产生的保护性反应效果更差。这表明NO在针对百日咳博德特氏菌攻击的保护作用中发挥重要作用。