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脂多糖诱导的黏膜固有免疫反应刺激可预防百日咳博德特氏菌定植。

Mucosal innate response stimulation induced by lipopolysaccharide protects against Bordetella pertussis colonization.

机构信息

Facultad de Ciencias Exactas, Laboratorio de Investigaciones del Sistema Inmune (LISIN), UNLP 47 y 115, 1900, La Plata, Argentina.

出版信息

Med Microbiol Immunol. 2010 May;199(2):103-8. doi: 10.1007/s00430-010-0142-5. Epub 2010 Feb 9.

DOI:10.1007/s00430-010-0142-5
PMID:20143087
Abstract

Non-specific enhancement of the airways innate response has been shown to impair lung infections in several models of infection such diverse as influenza A, Streptococcus pneumoniae, and Aspergillus niger. Our aim was to evaluate whether a similar event could operate in the context of Bordetella pertussis respiratory infection, not only to enrich the knowledge of host-bacteria interaction but also to establish immunological basis for the development of new control strategies against the pathogen. Using a B. pertussis intranasal infection model and coadministration of different TLR agonists at the moment of the infection, we observed that the enhancement of innate response activation, in a TLR4-dependent way, could efficiently impair B. pertussis colonization (P < 0.001). While LPS from different microbial sources were equally effective in promoting this effect, flagellin and poly I:C coadministration, in spite of inducing expression of innate response markers TNFalpha, CXCL2, CXCL10 and IL6, was not effective to prevent B. pertussis colonization. Our results indicate that during the early stage of infection, specific anti-microbial mechanisms triggered by TLR4 stimulation are able to impair B. pertussis colonization. These findings could complement our current view of the role of TLR4-dependent processes that contribute to anti-pertussis immunity.

摘要

非特异性增强气道先天反应已被证明可损害多种感染模型中的肺部感染,如流感 A、肺炎链球菌和黑曲霉。我们的目的是评估在百日咳博德特氏菌呼吸道感染的背景下是否会发生类似的事件,这不仅丰富了宿主-细菌相互作用的知识,而且为开发针对病原体的新控制策略奠定了免疫学基础。使用百日咳博德特氏菌鼻内感染模型和在感染时同时给予不同 TLR 激动剂,我们观察到先天反应激活的增强(以 TLR4 依赖性方式)可有效抑制百日咳博德特氏菌定植(P < 0.001)。虽然来自不同微生物来源的 LPS 在促进这种作用方面同样有效,但鞭毛蛋白和聚 I:C 共同给药虽然诱导了先天反应标志物 TNFalpha、CXCL2、CXCL10 和 IL6 的表达,但不能有效预防百日咳博德特氏菌定植。我们的结果表明,在感染的早期阶段,TLR4 刺激引发的特定抗微生物机制能够抑制百日咳博德特氏菌的定植。这些发现可以补充我们目前对 TLR4 依赖性过程在抗百日咳免疫中的作用的认识。

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本文引用的文献

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PLoS One. 2009 Oct 6;4(10):e7259. doi: 10.1371/journal.pone.0007259.
2
Stimulated innate resistance of lung epithelium protects mice broadly against bacteria and fungi.肺上皮细胞的天然抵抗刺激广泛保护小鼠免受细菌和真菌的侵害。
Am J Respir Cell Mol Biol. 2010 Jan;42(1):40-50. doi: 10.1165/rcmb.2008-0260OC. Epub 2009 Mar 27.
3
Activation of toll-like receptor signaling pathway for protection against influenza virus infection.
慢性肺部炎症可增强体液免疫并增强抗肺炎球菌的抵抗力。
Sci Rep. 2017 Jul 10;7(1):4972. doi: 10.1038/s41598-017-05212-4.
4
New aspects of RpoE in uropathogenic Proteus mirabilis.奇异变形杆菌中RpoE在泌尿道致病性方面的新情况。
Infect Immun. 2015 Mar;83(3):966-77. doi: 10.1128/IAI.02232-14. Epub 2014 Dec 29.
5
Bordetella pertussis naturally occurring isolates with altered lipooligosaccharide structure fail to fully mature human dendritic cells.脂寡糖结构改变的百日咳博德特氏菌自然分离株无法使人类树突状细胞完全成熟。
Infect Immun. 2015 Jan;83(1):227-38. doi: 10.1128/IAI.02197-14. Epub 2014 Oct 27.
6
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Recent publications in medical microbiology and immunology: a retrospective.医学微生物学与免疫学近期出版物:回顾。
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