Evidence map›Paper›PMID 22802341›Full record

ArticleInfection and immunity2012

NlpI facilitates deposition of C4bp on Escherichia coli by blocking classical complement-mediated killing, which results in high-level bacteremia.

Yu-ting Tseng, Shainn-Wei Wang, Kwang Sik Kim, Ying-Hsiang Wang, Yufeng Yao, Chien-Cheng Chen, Chi-Wu Chiang, Pao-Chuan Hsieh, Ching-Hao Teng

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.0field-weighted citation impact, top 25% of its field
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

22 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Survival ofPathogens (Basel, Switzerland) · 2024
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  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. An ArcA-Modulated Small RNA in PathogenicFrontiers in microbiology · 2020
    Article
  11. Peptidoglycan Endopeptidase Spr of UropathogenicFrontiers in microbiology · 2020
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. HowFrontiers in immunology · 2017
    Review
  17. Innate immune evasion of Escherichia coli clinical strains from orthopedic implant infections.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2016
    Article
  18. Review
  19. Multifunctional and Redundant Roles ofFrontiers in immunology · 2016
    Review
  20. Article
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

9 authors at 6 institutions in 3 countries.

Yu-ting TsengInstitute of Molecular Medicine, National Cheng Kung University Medical College, Tainan City, Taiwan.
Shainn-Wei Wang
Kwang Sik Kim
Ying-Hsiang Wang
Yufeng Yao
Chien-Cheng Chen
Chi-Wu Chiang
Pao-Chuan Hsieh
Ching-Hao Teng
National Cheng Kung University · TWChang Gung University · TWJohns Hopkins Medicine · USNational Kaohsiung Normal University · TWNational Pingtung University of Science and Technology · TWShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neonatal meningitis Escherichia coli (NMEC) is the most common Gram-negative organism that is associated with neonatal meningitis, which usually develops as a result of hematogenous spread of the bacteria. There are two key pathogenesis processes for NMEC to penetrate into the brain, the essential step for the development of E. coli meningitis: a high-level bacteremia and traversal of the blood-brain barrier (BBB). Our previous study has shown that the bacterial outer membrane protein NlpI contributes to NMEC binding to and invasion of brain microvascular endothelial cells, the major component cells of the BBB, suggesting a role for NlpI in NMEC crossing of the BBB. In this study, we showed that NlpI is involved in inducing a high level of bacteremia. In addition, NlpI contributed to the recruitment of the complement regulator C4bp to the surface of NMEC to evade serum killing, which is mediated by the classical complement pathway. NlpI may be involved in the interaction between C4bp and OmpA, which is an outer membrane protein that directly interacts with C4bp on the bacterial surface. The involvement of NlpI in two key pathogenesis processes of NMEC meningitis may make this bacterial factor a potential target for prevention and therapy of E. coli meningitis.

Indexed as

AnimalsAnimals, NewbornBacteremiaComplement C3bComplement Pathway, ClassicalDisease Models, AnimalEscherichia coliEscherichia coli InfectionsEscherichia coli ProteinsGene Expression Regulation, BacterialHistocompatibility AntigensHumansLipoproteinsMiceMutationNeutrophilsC4bp protein, mouseComplement C3bEscherichia coli ProteinsHistocompatibility AntigensLipoproteinsNlpI protein, E coli

Identifiers

PMID22802341
PMCPMC3457581
OpenAlexW2140651023

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.