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支气管败血波氏杆菌III型分泌系统抑制γ干扰素的产生,而γ干扰素是有效抗体介导的细菌清除所必需的。

The Bordetella bronchiseptica type III secretion system inhibits gamma interferon production that is required for efficient antibody-mediated bacterial clearance.

作者信息

Pilione Mylisa R, Harvill Eric T

机构信息

Department of Veterinary and Biomedical Science, The Pennsylvania State University, 115 Henning, University Park, PA 16802, USA.

出版信息

Infect Immun. 2006 Feb;74(2):1043-9. doi: 10.1128/IAI.74.2.1043-1049.2006.

DOI:10.1128/IAI.74.2.1043-1049.2006
PMID:16428751
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1360352/
Abstract

Several species of pathogenic microorganisms have developed strategies to survive and persist in vital organs which are normally maintained as sterile by the generation of strong immune responses. Here, we report an immunomodulation involving the Bordetella bronchiseptica type III secretion system (TTSS) which contributes to bacterial survival in the lower respiratory tract of the host. The prolonged persistence of B. bronchiseptica that was observed in gamma interferon (IFN-gamma)-/- mice indicates that the efficient clearance of bacteria from the lower respiratory tract requires not only B cells and antibodies but also IFN-gamma production. Our data also suggest that interleukin-10 (IL-10)-producing splenocytes are generated early during infection and that IL-10 inhibits IFN-gamma-producing cells and delays the clearance of B. bronchiseptica from the lungs. The TTSS of B. bronchiseptica inhibits the generation of IFN-gamma-producing splenocytes and is required for long-term bacterial persistence in the lower respiratory tract in wild-type mice. This suggests that a mechanism involving the modulation of IFN-gamma production by the TTSS facilitates B. bronchiseptica survival in the lower respiratory tract.

摘要

几种致病微生物已经形成了在重要器官中存活和持续存在的策略,而这些重要器官通常通过产生强烈的免疫反应来保持无菌状态。在此,我们报告了一种涉及支气管败血博德特氏菌III型分泌系统(TTSS)的免疫调节作用,该系统有助于细菌在宿主下呼吸道中存活。在γ干扰素(IFN-γ)基因敲除小鼠中观察到支气管败血博德特氏菌的长期持续存在,这表明从下呼吸道有效清除细菌不仅需要B细胞和抗体,还需要产生IFN-γ。我们的数据还表明,在感染早期会产生产生白细胞介素10(IL-10)的脾细胞,并且IL-10会抑制产生IFN-γ的细胞,并延迟支气管败血博德特氏菌从肺部的清除。支气管败血博德特氏菌的TTSS会抑制产生IFN-γ的脾细胞的生成,并且是野生型小鼠下呼吸道中细菌长期持续存在所必需的。这表明一种涉及TTSS调节IFN-γ产生的机制促进了支气管败血博德特氏菌在下呼吸道中的存活。

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The Bordetella bronchiseptica type III secretion system inhibits gamma interferon production that is required for efficient antibody-mediated bacterial clearance.支气管败血波氏杆菌III型分泌系统抑制γ干扰素的产生,而γ干扰素是有效抗体介导的细菌清除所必需的。
Infect Immun. 2006 Feb;74(2):1043-9. doi: 10.1128/IAI.74.2.1043-1049.2006.
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本文引用的文献

1
The complex mechanism of antibody-mediated clearance of Bordetella from the lungs requires TLR4.抗体介导的从肺部清除博德特氏菌的复杂机制需要Toll样受体4(TLR4)。
J Immunol. 2005 Dec 1;175(11):7504-11. doi: 10.4049/jimmunol.175.11.7504.
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Bordetella type III secretion modulates dendritic cell migration resulting in immunosuppression and bacterial persistence.博德特氏菌III型分泌调节树突状细胞迁移,导致免疫抑制和细菌持续存在。
J Immunol. 2005 Oct 1;175(7):4647-52. doi: 10.4049/jimmunol.175.7.4647.
3
Bordetella type III secretion and adenylate cyclase toxin synergize to drive dendritic cells into a semimature state.博德特氏菌III型分泌系统与腺苷酸环化酶毒素协同作用,促使树突状细胞进入半成熟状态。
J Immunol. 2004 Aug 1;173(3):1934-40. doi: 10.4049/jimmunol.173.3.1934.
4
pagP is required for resistance to antibody-mediated complement lysis during Bordetella bronchiseptica respiratory infection.支气管败血波氏杆菌呼吸道感染期间,抗抗体介导的补体溶解作用需要pagP。
Infect Immun. 2004 May;72(5):2837-42. doi: 10.1128/IAI.72.5.2837-2842.2004.
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Interferon-gamma activation of polymorphonuclear neutrophil function.γ干扰素对多形核中性粒细胞功能的激活作用。
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6
Adenylate cyclase toxin from Bordetella pertussis synergizes with lipopolysaccharide to promote innate interleukin-10 production and enhances the induction of Th2 and regulatory T cells.百日咳博德特氏菌的腺苷酸环化酶毒素与脂多糖协同作用,促进先天性白细胞介素-10的产生,并增强Th2细胞和调节性T细胞的诱导。
Infect Immun. 2004 Mar;72(3):1568-79. doi: 10.1128/IAI.72.3.1568-1579.2004.
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Antibody-mediated bacterial clearance from the lower respiratory tract of mice requires complement component C3.抗体介导的细菌从小鼠下呼吸道清除需要补体成分C3。
Eur J Immunol. 2004 Jan;34(1):184-93. doi: 10.1002/eji.200324234.
8
Hepatitis C virus non-structural protein 4 suppresses Th1 responses by stimulating IL-10 production from monocytes.丙型肝炎病毒非结构蛋白4通过刺激单核细胞产生白细胞介素-10来抑制Th1反应。
Eur J Immunol. 2003 Dec;33(12):3448-57. doi: 10.1002/eji.200324251.
9
Toll-like receptor 4-mediated innate IL-10 activates antigen-specific regulatory T cells and confers resistance to Bordetella pertussis by inhibiting inflammatory pathology.Toll样受体4介导的固有白细胞介素-10激活抗原特异性调节性T细胞,并通过抑制炎症病理反应赋予对百日咳博德特氏菌的抗性。
J Immunol. 2003 Sep 15;171(6):3119-27. doi: 10.4049/jimmunol.171.6.3119.
10
Bordetella bronchiseptica PagP is a Bvg-regulated lipid A palmitoyl transferase that is required for persistent colonization of the mouse respiratory tract.支气管败血波氏杆菌PagP是一种受Bvg调控的脂多糖A棕榈酰转移酶,是小鼠呼吸道持续定植所必需的。
Mol Microbiol. 2003 May;48(3):725-36. doi: 10.1046/j.1365-2958.2003.03484.x.