Evidence map›Paper›PMID 26426079›Full record

ArticleThe Journal of clinical investigation2015

Bacterial exploitation of phosphorylcholine mimicry suppresses inflammation to promote airway infection.

Christopher B Hergott, Aoife M Roche, Nikhil A Naidu, Clementina Mesaros, Ian A Blair, Jeffrey N Weiser

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

19 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. Phosphocholine decoration ofCell surface (Amsterdam, Netherlands) · 2022
    Article
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  5. Article
  6. Article
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  8. Review
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  10. Review
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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

6 authors at 3 institutions in 2 countries.

Christopher B Hergott
Aoife M Roche
Nikhil A Naidu
Clementina Mesaros
Ian A Blair
Jeffrey N Weiser
Czech Academy of Sciences, Institute of Microbiology · CZTranslational Therapeutics (United States) · USNew York University · US

Funding

UNIVERSITY OF PENNSYLVANIA CAN CTR SUPPORT GRANTP30CA016520 · NCI · UNIVERSITY OF PENNSYLVANIA · PI SHELLEY L BERGER · 1985 to 2026
$222.3M
Translational Research Support CoreP30ES013508 · NIEHS · UNIVERSITY OF PENNSYLVANIA · PI Rebecca A Simmons · 2006 to 2026
$35.3M
ROLE OF OPACITY VARIATION IN PNEUMOCOCCAL PATHOGENESISR01AI038446 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI WEISER, JEFFREY NEAL · 1996 to 2019
$7.4M
Mechanisms of Pneumococcal Persistence During CarriageR37AI038446 · NIAID · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI Jeffrey Neal Weiser · 2020 to 2026
$3.8M
Early Events in Pneumococcal ColonizationR01AI105168 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI WEISER, JEFFREY NEAL · 2014 to 2018
$2.1M
Training in bacteriologyT32AI060516 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI GOULIAN, MARK D, ZHU, JUN · 2006 to 2015
$2.0M
NCI NIH HHS P30 CA016520NCI NIH HHS P30CA016520NIAID NIH HHS AI038446NIAID NIH HHS AI060516NIAID NIH HHS AI105168NIAID NIH HHS R01 AI038446NIAID NIH HHS R01 AI105168NIAID NIH HHS R37 AI038446NIAID NIH HHS T32 AI060516NIEHS NIH HHS P30 ES013508
6 · The paper itself

Abstract

Regulation of neutrophil activity is critical for immune evasion among extracellular pathogens, yet the mechanisms by which many bacteria disrupt phagocyte function remain unclear. Here, we have shown that the respiratory pathogen Streptococcus pneumoniae disables neutrophils by exploiting molecular mimicry to degrade platelet-activating factor (PAF), a host-derived inflammatory phospholipid. Using mass spectrometry and murine upper airway infection models, we demonstrated that phosphorylcholine (ChoP) moieties that are shared by PAF and the bacterial cell wall allow S. pneumoniae to leverage a ChoP-remodeling enzyme (Pce) to remove PAF from the airway. S. pneumoniae-mediated PAF deprivation impaired viability, activation, and bactericidal capacity among responding neutrophils. In the absence of Pce, neutrophils rapidly cleared S. pneumoniae from the airway and impeded invasive disease and transmission between mice. Abrogation of PAF signaling rendered Pce dispensable for S. pneumoniae persistence, reinforcing that this enzyme deprives neutrophils of essential PAF-mediated stimulation. Accordingly, exogenous activation of neutrophils overwhelmed Pce-mediated phagocyte disruption. Haemophilus influenzae also uses an enzyme, GlpQ, to hydrolyze ChoP and subvert PAF function, suggesting that mimicry-driven immune evasion is a common paradigm among respiratory pathogens. These results identify a mechanism by which shared molecular structures enable microbial enzymes to subvert host lipid signaling, suppress inflammation, and ensure bacterial persistence at the mucosa.

Indexed as

Molecular MimicryAnimalsBacterial ProteinsCarrier ProteinsCarrier StateCell WallHaemophilus InfectionsHaemophilus influenzaeHumansImmune EvasionImmunity, InnateImmunoglobulin DLipoproteinsMiceMice, Inbred C57BLMice, KnockoutBacterial ProteinsCarrier Proteinscholine-binding protein E, Streptococcus pneumoniaeglpQ protein, Haemophilus influenzaeImmunoglobulin DLipoproteinsN-Formylmethionine Leucyl-PhenylalaninePhosphorylcholinePlatelet Activating Factorplatelet activating factor receptorPlatelet Membrane GlycoproteinsReceptors, Cell SurfaceReceptors, G-Protein-Coupled

Identifiers

PMID26426079
PMCPMC4607119
OpenAlexW2170852538

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.