Evidence map›Paper›PMID 30190495›Full record

ArticleScientific reports2018

Characterization of lasR-deficient clinical isolates of Pseudomonas aeruginosa.

Yao Wang, Leiqiong Gao, Xiancai Rao, Jing Wang, Hua Yu, Junru Jiang, Wei Zhou, Jin Wang, Yonghong Xiao, Mengwen Li and 4 more

Abstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

36 citing papers in PubMed.

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  12. Spread ofAntibiotics (Basel, Switzerland) · 2023
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  15. Article
  16. Article
  17. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors.

Yao WangDepartment of Neonatology, Children's Hospital of Chongqing Medical University, Ministry of Education Key Laboratory of Child Development and Disorders, China International Science and Technology Cooperation base of Child development and Critical Disorders, Chongqing Key Laboratory of Child Infection and Immunity, Chongqing, 40014, China.
Leiqiong GaoDepartment of Neonatology, Children's Hospital of Chongqing Medical University, Ministry of Education Key Laboratory of Child Development and Disorders, China International Science and Technology Cooperation base of Child development and Critical Disorders, Chongqing Key Laboratory of Child Infection and Immunity, Chongqing, 40014, China.
Xiancai RaoDepartment of Microbiology, Army Medical University, Chongqing, 400038, China.ORCID 0000-0002-9905-760X
Jing WangDepartment of Neonatology, Children's Hospital of Chongqing Medical University, Ministry of Education Key Laboratory of Child Development and Disorders, China International Science and Technology Cooperation base of Child development and Critical Disorders, Chongqing Key Laboratory of Child Infection and Immunity, Chongqing, 40014, China.
Hua YuDepartment of Central Laboratory, Xinqiao Hospital, Army Medical University, Chongqing, China.
Junru JiangDepartment of Neonatology, Children's Hospital of Chongqing Medical University, Ministry of Education Key Laboratory of Child Development and Disorders, China International Science and Technology Cooperation base of Child development and Critical Disorders, Chongqing Key Laboratory of Child Infection and Immunity, Chongqing, 40014, China.
Wei ZhouDepartment of Neonatology, Children's Hospital of Chongqing Medical University, Ministry of Education Key Laboratory of Child Development and Disorders, China International Science and Technology Cooperation base of Child development and Critical Disorders, Chongqing Key Laboratory of Child Infection and Immunity, Chongqing, 40014, China.
Jin WangPhase I Clinical Centre, Beijing Shijitan Hospital, Capital Medical University, Beijing, 100038, China.
Yonghong XiaoCollaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China, 300013.
Mengwen LiDepartment of Neonatology, Children's Hospital of Chongqing Medical University, Ministry of Education Key Laboratory of Child Development and Disorders, China International Science and Technology Cooperation base of Child development and Critical Disorders, Chongqing Key Laboratory of Child Infection and Immunity, Chongqing, 40014, China.
Yan ZhangDepartment of Neonatology, Children's Hospital of Chongqing Medical University, Ministry of Education Key Laboratory of Child Development and Disorders, China International Science and Technology Cooperation base of Child development and Critical Disorders, Chongqing Key Laboratory of Child Infection and Immunity, Chongqing, 40014, China.
Kebin ZhangDepartment of Central Laboratory, Xinqiao Hospital, Army Medical University, Chongqing, China.
Li ShenDepartment of Microbiology, Immunology, and Parasitology, Louisiana State University Health Sciences Center, New Orleans, LA, 70112, USA. lshen@lsuhsc.edu.
Ziyu HuaDepartment of Neonatology, Children's Hospital of Chongqing Medical University, Ministry of Education Key Laboratory of Child Development and Disorders, China International Science and Technology Cooperation base of Child development and Critical Disorders, Chongqing Key Laboratory of Child Infection and Immunity, Chongqing, 40014, China. h_ziyu@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pseudomonas aeruginosa is a prevalent opportunistic pathogen that causes fatal infections in immunocompromised individuals. Quorum sensing (QS) is a cell-to-cell communication process that controls virulence gene expression and biofilm formation in P. aeruginosa. Here, the QS systems and the relevant virulence traits in clinical P. aeruginosa isolates were characterized. Eleven out of the ninety-four P. aeruginosa isolates exhibited a biofilm-deficient phenotype. Two biofilm-deficient isolates, one from blood and the one from pleural effusion, appeared to carry a same mutation in lasR. These two isolates differed in the ability to produce QS-regulated virulence factors, but contained the same functionally deficient LasR with the truncated C-terminal domains and belonged to the same multilocus sequence type (ST227). Chromosomal lasR complementation in these lasR mutants verified that lasR inactivation was the sole cause of las deficiency. LasR was not absolutely required for rhl signal in these lasR mutants, suggesting the presence of lasR-independent QS systems. We provided evidence that the virulence gene expression are not regulated in the same manner in these isolates. These results support the hypothesis that conventional QS hierarchy can be smashed by naturally occurring lasR mutation in clinical P. aeruginosa isolates and that complex QS hierarchy may play a role in maintaining infection of this opportunistic pathogen.

Indexed as

Bacterial ProteinsMutationPseudomonas aeruginosaPseudomonas InfectionsTranscription FactorsVirulence FactorsHumansQuorum SensingBacterial ProteinsTranscription FactorsVirulence Factors

Identifiers

PMID30190495
PMCPMC6127196

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.