Higher Prevalence of PldA, a Pseudomonas aeruginosa Trans-Kingdom H2-Type VI Secretion System Effector, in Clinical Isolates Responsible for Acute Infections and in Multidrug Resistant Strains.

Higher Prevalence of PldA, a Pseudomonas aeruginosa Trans-Kingdom H2-Type VI Secretion System Effector, in Clinical Isolates Responsible for Acute Infections and in Multidrug Resistant Strains.
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DOI:
10.3389/fmicb.2018.02578
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发表时间:
2018
影响因子:
5.2
通讯作者:
Dortet L
Dortet L
中科院分区:
生物学2区
文献类型:
--
作者:
Boulant T;Boudehen YM;Filloux A;Plesiat P;Naas T;Dortet L

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铜绿假单胞菌可以使用由III型或VI型分泌系统(T3 SS和T6 SS)递送的分泌效应物操纵真核宿主细胞。T3 SS允许将细菌效应物(外毒素)注射到真核细胞中。铜绿假单胞菌编码三种T6 SS,H1-、H2-和H3-T6 SS。H1-T6 SS主要参与传递毒素以杀死细菌竞争对手。最近,两种T6 SS分泌的磷脂酶D,PldA(H2-T6 SS)和PldB(H3-T6 SS),被鉴定为跨界毒力效应物,触发杀死细菌竞争者和内化到非吞噬细胞中。我们在185个临床分离株(败血症、肺部感染、尿路感染和CF患者的慢性感染)、47个环境菌株和33个碳青霉烯酶产生菌中破译了T3 SS和T6 SS效应子编码基因的流行率。我们纳入了公共数据库中的107个完整的铜绿假单胞菌基因组。pldA的流行率在导致严重急性感染的临床分离株中增加,特别是在多药耐药菌株中。相比之下,pldB患病率在所有分离株中均较高(96.8%)。关于T3 SS效应子,exoT和exoY存在于几乎所有分离株中,而exoS和exoU被发现是排他性的,在严重急性感染中exoU+菌株的患病率较高。高毒力exoU+分离株更倾向于pldA+,表明PldA在毒力中的作用。最后,我们观察到产生IMP型碳青霉烯酶的极端耐药分离株均为pldA+。我们的研究结果表明,PldA可能在肺部感染过程中发挥作用,并在多药耐药菌株,特别是IMP生产者中共同选择。
Pseudomonas aeruginosa can manipulate eukaryotic host cells using secreted effectors delivered by the type III or the type VI Secretion Systems (T3SS and T6SS). The T3SS allows the injection of bacterial effectors (Exo toxins) into eukaryotic cell. P. aeruginosa, encodes three T6SSs, H1-, H2- and H3-T6SS. The H1-T6SS is mainly involved in delivering toxins to kill bacterial competitors. Recently, two T6SS-secreted phospholipases D, PldA (H2-T6SS) and PldB (H3-T6SS), were identified as trans-kingdom virulence effectors, triggering both killing of bacterial competitors and internalization into non-phagocytic cells. We deciphered the prevalence of T3SS and T6SS effectors encoding genes in 185 clinical isolates responsible for infections (septicaemia, pulmonary infections, urinary tract infections, and chronic infections in CF patients), 47 environmental strains, and on 33 carbapenemase-producers. We included 107 complete genomes of P. aeruginosa available in public databases. The prevalence of pldA is increased in clinical isolates responsible for severe acute infection and particularly in multi-drug resistant strains. In contrast, the pldB prevalence was high (96.8%) in all isolates. Regarding T3SS effectors, exoT and exoY are present in nearly all isolates while exoS and exoU were found to be exclusive with a higher prevalence of exoU+ strains in severe acute infections. The hypervirulent exoU+ isolates are more prone to be pldA+, suggesting a role of PldA in virulence. Finally, we observed that extremely drug resistant isolates producing an IMP-type carbapenemase were all pldA+. Our results suggest that PldA might have a role during pulmonary infections and have been co-selected in multidrug resistant strains particularly IMP-producers.
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