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本文引用的文献

1
Single-molecule atomic force microscopy unravels the binding mechanism of a Burkholderia cenocepacia trimeric autotransporter adhesin.单分子原子力显微镜揭示了伯克霍尔德氏菌属三联体自转运黏附素的结合机制。
Mol Microbiol. 2013 Aug;89(4):649-59. doi: 10.1111/mmi.12301. Epub 2013 Jul 12.
2
Anti-adhesion methods as novel therapeutics for bacterial infections.抗黏附方法:细菌感染的新型治疗策略。
Expert Rev Anti Infect Ther. 2012 Dec;10(12):1457-68. doi: 10.1586/eri.12.145.
3
Complete fiber structures of complex trimeric autotransporter adhesins conserved in enterobacteria.完整的纤维结构,复杂三聚体自转运黏附素,在肠杆菌中保守。
Proc Natl Acad Sci U S A. 2012 Dec 18;109(51):20907-12. doi: 10.1073/pnas.1211872110. Epub 2012 Dec 3.
4
Trimeric autotransporter adhesins in members of the Burkholderia cepacia complex: a multifunctional family of proteins implicated in virulence.伯克霍尔德氏菌复合群成员中的三聚体自转运黏附素:一种与毒力相关的多功能蛋白家族。
Front Cell Infect Microbiol. 2011 Dec 7;1:13. doi: 10.3389/fcimb.2011.00013. eCollection 2011.
5
A BCAM0223 mutant of Burkholderia cenocepacia is deficient in hemagglutination, serum resistance, adhesion to epithelial cells and virulence.伯克霍尔德氏菌中 ABCAM0223 突变体在血凝、血清抗性、黏附上皮细胞和毒力方面存在缺陷。
PLoS One. 2012;7(7):e41747. doi: 10.1371/journal.pone.0041747. Epub 2012 Jul 25.
6
Evaluation of the trimeric autotransporter Ata as a vaccine candidate against Acinetobacter baumannii infections.评估三聚体自转运蛋白 Ata 作为治疗鲍曼不动杆菌感染的疫苗候选物。
Infect Immun. 2012 Oct;80(10):3381-8. doi: 10.1128/IAI.06096-11. Epub 2012 Jul 23.
7
Molecular characterization of the EhaG and UpaG trimeric autotransporter proteins from pathogenic Escherichia coli.致病性大肠杆菌 EhaG 和 UpaG 三聚体自转运蛋白的分子特征。
Appl Environ Microbiol. 2012 Apr;78(7):2179-89. doi: 10.1128/AEM.06680-11. Epub 2012 Jan 27.
8
SadA, a trimeric autotransporter from Salmonella enterica serovar Typhimurium, can promote biofilm formation and provides limited protection against infection.沙门氏菌血清型鼠伤寒的三聚体自转运蛋白 SadA 能够促进生物膜的形成,并对感染提供有限的保护。
Infect Immun. 2011 Nov;79(11):4342-52. doi: 10.1128/IAI.05592-11. Epub 2011 Aug 22.
9
Structure and biology of trimeric autotransporter adhesins.三聚体自转运黏附素的结构与生物学。
Adv Exp Med Biol. 2011;715:143-58. doi: 10.1007/978-94-007-0940-9_9.
10
Burkholderia cenocepacia in cystic fibrosis: epidemiology and molecular mechanisms of virulence.西地西菌属在囊性纤维化中的作用:流行病学和毒力的分子机制。
Clin Microbiol Infect. 2010 Jul;16(7):821-30. doi: 10.1111/j.1469-0691.2010.03237.x.

鉴定人体病原体洋葱伯克霍尔德氏菌的多功能三聚体自转运蛋白 BCAM0224。

Characterization of BCAM0224, a multifunctional trimeric autotransporter from the human pathogen Burkholderia cenocepacia.

机构信息

IBB-Institute for Biotechnology and Bioengineering, Instituto Superior Técnico, Lisbon, Portugal.

出版信息

J Bacteriol. 2014 Jun;196(11):1968-79. doi: 10.1128/JB.00061-14. Epub 2014 Mar 21.

DOI:10.1128/JB.00061-14
PMID:24659767
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4010975/
Abstract

Members of the trimeric autotransporter adhesin (TAA) family play a crucial role in adhesion of Gram-negative pathogens to host cells. Moreover, these proteins are multifunctional virulence factors involved in several other biological traits, including invasion into host cells and evasion of the host immune system. In cystic fibrosis epidemic Burkholderia cenocepacia strain J2315, we identified a unique TAA (BCAM0224)-encoding gene, previously described as being implicated in virulence. Here, we characterized this multifunctional protein, trying to establish its role in B. cenocepacia pathogenicity. We show that BCAM0224 occurs on the bacterial surface and adopts a trimeric conformation. Furthermore, we demonstrated that BCAM0224 is needed for earlier stages of biofilm formation and is required for swarming motility. In addition, BCAM0224 plays an important role in evasion of the human innate immune system, providing resistance against the bactericidal activity of serum via the complement classical pathway. Finally, BCAM0224 mediates bacterial adhesion to and invasion of cultured human bronchial epithelial cells. Together, these data reveal the high versatility of the BCAM0224 protein as a virulence factor in the pathogenic bacterium B. cenocepacia.

摘要

三聚体自转运黏附素(TAA)家族的成员在革兰氏阴性病原体与宿主细胞黏附中起着至关重要的作用。此外,这些蛋白是多功能毒力因子,参与多种其他生物学特性,包括入侵宿主细胞和逃避宿主免疫系统。在囊性纤维化流行的伯克霍尔德氏菌中,我们鉴定了一个独特的 TAA(BCAM0224)编码基因,该基因先前被描述为与毒力有关。在这里,我们对这种多功能蛋白进行了表征,试图确定其在伯克霍尔德氏菌致病性中的作用。我们表明,BCAM0224 存在于细菌表面并采用三聚体构象。此外,我们证明 BCAM0224 是生物膜形成早期所必需的,并且是群集运动所必需的。此外,BCAM0224 在逃避人体先天免疫系统方面发挥着重要作用,通过补体经典途径提供对血清杀菌活性的抗性。最后,BCAM0224 介导细菌对培养的人支气管上皮细胞的黏附和入侵。总之,这些数据揭示了 BCAM0224 蛋白作为致病性细菌伯克霍尔德氏菌的毒力因子的高度多功能性。