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TIR结构域基因是促进细菌在血液中存活的基因簇的一部分。

TIR-Domain Genes Are Part of a Gene Cluster Which Promotes Bacterial Survival in Blood.

作者信息

Wagner Theresa M, Janice Jessin, Paganelli Fernanda L, Willems Rob J, Askarian Fatemeh, Pedersen Torunn, Top Janetta, de Haas Carla, van Strijp Jos A, Johannessen Mona, Hegstad Kristin

机构信息

Research Group for Host-Microbe Interactions, Department of Medical Biology, Faculty of Health Sciences, UiT-The Arctic University of Norway, Tromsø, Norway.

Norwegian National Advisory Unit on Detection of Antimicrobial Resistance, Department of Microbiology and Infection Control, University Hospital of North-Norway, Tromsø, Norway.

出版信息

Int J Microbiol. 2018 Dec 3;2018:1435820. doi: 10.1155/2018/1435820. eCollection 2018.

DOI:10.1155/2018/1435820
PMID:30631364
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6304867/
Abstract

has undergone a transition to a multidrug-resistant nosocomial pathogen. The population structure of is characterized by a sharp distinction of clades, where the hospital-adapted lineage is primarily responsible for bacteremia. So far, factors that were identified in hospital-adapted strains and that promoted pathogenesis of nosocomial mainly play a role in adherence and biofilm production, while less is known about factors contributing to survival in blood. This study identified a gene cluster, which includes genes encoding bacterial Toll/interleukin-1 receptor- (TIR-) domain-containing proteins (TirEs). The cluster was found to be unique to nosocomial strains and to be located on a putative mobile genetic element of phage origin. The three genes within the cluster appeared to be expressed as an operon. Expression was detected in bacterial culture media and in the presence of human blood. TirEs are released into the bacterial supernatant, and TirE2 is associated with membrane vesicles. Furthermore, the -gene cluster promotes bacterial proliferation in human blood, indicating that TirE may contribute to the pathogenesis of bacteremia.

摘要

已转变为多重耐药的医院病原体。其群体结构的特点是进化枝有明显区别,其中适应医院环境的谱系主要导致菌血症。到目前为止,在适应医院环境的菌株中鉴定出的、促进医院感染发病机制的因素主要在黏附和生物膜形成中起作用,而关于促成在血液中存活的因素了解较少。本研究鉴定出一个基因簇,其中包括编码含细菌Toll/白细胞介素-1受体(TIR)结构域蛋白(TirEs)的基因。该基因簇被发现是医院菌株所特有的,并且位于一个推测的噬菌体起源的可移动遗传元件上。该基因簇内的三个基因似乎作为一个操纵子表达。在细菌培养基和人血液存在的情况下检测到了表达。TirEs被释放到细菌上清液中,并且TirE2与膜泡相关。此外,该基因簇促进细菌在人血液中的增殖,表明TirE可能促成菌血症的发病机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d56c/6304867/fbca833501a0/IJMICRO2018-1435820.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d56c/6304867/b761ab25408e/IJMICRO2018-1435820.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d56c/6304867/6a136a23e4d8/IJMICRO2018-1435820.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d56c/6304867/e326a4486f48/IJMICRO2018-1435820.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d56c/6304867/3c3769b64481/IJMICRO2018-1435820.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d56c/6304867/cfea15db5048/IJMICRO2018-1435820.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d56c/6304867/0973d3abcebc/IJMICRO2018-1435820.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d56c/6304867/52cdebe17ddd/IJMICRO2018-1435820.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d56c/6304867/fbca833501a0/IJMICRO2018-1435820.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d56c/6304867/b761ab25408e/IJMICRO2018-1435820.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d56c/6304867/6a136a23e4d8/IJMICRO2018-1435820.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d56c/6304867/e326a4486f48/IJMICRO2018-1435820.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d56c/6304867/3c3769b64481/IJMICRO2018-1435820.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d56c/6304867/cfea15db5048/IJMICRO2018-1435820.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d56c/6304867/0973d3abcebc/IJMICRO2018-1435820.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d56c/6304867/52cdebe17ddd/IJMICRO2018-1435820.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d56c/6304867/fbca833501a0/IJMICRO2018-1435820.008.jpg

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