Evidence map›Paper›PMID 19180241›Full record

ArticlePLoS pathogens2009

Local inflammation induces complement crosstalk which amplifies the antimicrobial response.

Jing Zhang, Jingyun Koh, Jinhua Lu, Steffen Thiel, Benjamin S H Leong, Sunil Sethi, Cynthia Y X He, Bow Ho, Jeak L Ding

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
4.7field-weighted citation impact, top 5% 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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 97 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
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  7. The Role of Anti-mCRP Autoantibodies in Lupus Nephritis.Kidney diseases (Basel, Switzerland) · 2023
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  10. Polymorphisms of theFrontiers in immunology · 2021
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  15. Age-related variations in theCentral-European journal of immunology · 2018
    Article
  16. Review
  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

9 authors at 3 institutions in 2 countries.

Jing ZhangNUS Graduate School for Integrative Science and Engineering, National University of Singapore, Singapore.
Jingyun Koh
Jinhua Lu
Steffen Thiel
Benjamin S H Leong
Sunil Sethi
Cynthia Y X He
Bow Ho
Jeak L Ding
National University of Singapore · SGAarhus University · DKNational University Hospital · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

By eliciting inflammatory responses, the human immunosurveillance system notably combats invading pathogens, during which acute phase proteins (CRP and cytokines) are elevated markedly. However, the Pseudomonas aeruginosa is a persistent opportunistic pathogen prevalent at the site of local inflammation, and its acquisition of multiple antibiotic-resistance factors poses grave challenges to patient healthcare management. Using blood samples from infected patients, we demonstrate that P. aeruginosa is effectively killed in the plasma under defined local infection-inflammation condition, where slight acidosis and reduced calcium levels (pH 6.5, 2 mM calcium) typically prevail. We showed that this powerful antimicrobial activity is provoked by crosstalk between two plasma proteins; CRPratioL-ficolin interaction led to communication between the complement classical and lectin pathways from which two amplification events emerged. Assays for C4 deposition, phagocytosis, and protein competition consistently proved the functional significance of the amplification pathways in boosting complement-mediated antimicrobial activity. The infection-inflammation condition induced a 100-fold increase in CRPratioL-ficolin interaction in a pH- and calcium-sensitive manner. We conclude that the infection-induced local inflammatory conditions trigger a strong interaction between CRPratioL-ficolin, eliciting complement-amplification pathways which are autonomous and which co-exist with and reinforce the classical and lectin pathways. Our findings provide new insights into the host immune response to P. aeruginosa infection under pathological conditions and the potential development of new therapeutic strategies against bacterial infection.

Indexed as

Complement Pathway, ClassicalComplement Pathway, Mannose-Binding LectinBlood Bactericidal ActivityCalciumComplement C1qComplement C3Complement C4C-Reactive ProteinData Interpretation, StatisticalFicolinsHost-Pathogen InteractionsHumansHydrogen-Ion ConcentrationInflammationLectinsPhagocytosisCalciumComplement C1qComplement C3Complement C4C-Reactive ProteinFicolinsLectins

Identifiers

PMID19180241
PMCPMC2629585
OpenAlexW2040175795

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.