Evidence map›Paper›PMID 27039343›Full record

ArticleEuropean journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology2016

Innate immune evasion of Escherichia coli clinical strains from orthopedic implant infections.

L Crémet, A Broquet, C Jacqueline, C Chaillou, K Asehnoune, S Corvec, N Caroff

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Article in European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 29% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

  1. Pooled it
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  14. Frontiers in immunology · 2017
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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

7 authors at 2 institutions in 1 country.

L CrémetUFR de Médecine, EA3826, Thérapeutiques cliniques et expérimentales des infections, Université de Nantes, 1 rue G. Veil, 44000, Nantes, France.
A BroquetUFR de Médecine, EA3826, Thérapeutiques cliniques et expérimentales des infections, Université de Nantes, 1 rue G. Veil, 44000, Nantes, France.
C JacquelineUFR de Médecine, EA3826, Thérapeutiques cliniques et expérimentales des infections, Université de Nantes, 1 rue G. Veil, 44000, Nantes, France.
C ChaillouUFR de Médecine, EA3826, Thérapeutiques cliniques et expérimentales des infections, Université de Nantes, 1 rue G. Veil, 44000, Nantes, France.
K AsehnouneUFR de Médecine, EA3826, Thérapeutiques cliniques et expérimentales des infections, Université de Nantes, 1 rue G. Veil, 44000, Nantes, France.
S CorvecUFR de Médecine, EA3826, Thérapeutiques cliniques et expérimentales des infections, Université de Nantes, 1 rue G. Veil, 44000, Nantes, France.
N CaroffUFR de Médecine, EA3826, Thérapeutiques cliniques et expérimentales des infections, Université de Nantes, 1 rue G. Veil, 44000, Nantes, France. nathalie.caroff@univ-nantes.fr.
Nantes Université · FRCentre Hospitalier Universitaire de Nantes · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Escherichia coli is one of the first causes of Gram-negative orthopedic implant infections (OII). Those infections, usually hematogenous, mostly originate from the urinary tract. We investigated the strategies developed by E. coli in this context to evade host innate immune responses, i.e. complement and polymorphonuclear neutrophils (PMN). Twenty strains from OII were compared with 20 strains from bacteremia in patients with non-infected orthopedic implant. In both groups, 6/20 (30 %) strains lysed PMNs, due to the production of the pore-forming toxin α-hemolysin (HlyA). For the others, resistance to phagocytic killing by PMN was not significantly different between both groups. In contrast, resistance to complement-mediated serum killing was significantly higher in OII strains than in the others (65 % vs 10 %; P <0.001). In E. coli, different mechanisms have been involved in complement resistance. Here, serum resistance was not linked to a group 2 capsule, or a loss of outer membrane permeability, or the recruitment of the complement inhibitor C4bp, but was significantly associated with the synthesis of long-chain LPS, regardless of the O-antigen. Thus, serum resistance could promote seeding of peri-implant tissues by helping E. coli to either persist in blood and reach the site of infection or overcome localized complement activation.

Indexed as

Immune EvasionImmunity, InnateProsthesis-Related InfectionsBacteremiaCell SurvivalEscherichia coliEscherichia coli InfectionsHumansMultilocus Sequence TypingNeutrophilsPhylogenySerogroup

Identifiers

PMID27039343
OpenAlexW2318220600

What OpenQuestion holds

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Registered trials

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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.