Evidence map›Paper›PMID 31392789›Full record

ArticleJournal of leukocyte biology2019

Frontline Science: Escherichia coli use LPS as decoy to impair neutrophil chemotaxis and defeat antimicrobial host defense.

Yutaka Kondo, Carola Ledderose, Christian J Slubowski, Mahtab Fakhari, Yuka Sumi, Koichiro Sueyoshi, Ann-Katrin Bezler, Dilan Aytan, Mona Arbab, Wolfgang G Junger

Open access · greenAbstract read
In one paragraph

Article in Journal of leukocyte biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.6field-weighted citation impact, top 19% 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

16 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Mechanisms of host-bacterial interactions duringFrontiers in veterinary science · 2025
    Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Anti-Inflammatory Metabolites in the Pathogenesis of Bacterial Infection.Frontiers in cellular and infection microbiology · 2022
    Review
  13. Roles of mitochondria in neutrophils.Frontiers in immunology · 2022
    Review
  14. Purinergic Signalling in Group AFrontiers in immunology · 2022
    Article
  15. Review
  16. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 3 countries.

Yutaka KondoDepartment of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.
Carola LedderoseDepartment of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.
Christian J SlubowskiDepartment of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.
Mahtab FakhariDepartment of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.
Yuka SumiDepartment of Emergency and Critical Care Medicine, Juntendo University, Urayasu Hospital, Chiba, Japan.
Koichiro SueyoshiDepartment of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.
Ann-Katrin BezlerDepartment of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.
Dilan AytanDepartment of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.
Mona ArbabDepartment of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.
Wolfgang G JungerDepartment of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.
Beth Israel Deaconess Medical Center · USHarvard University · USJuntendo University Urayasu Hospital · JP

Funding

Neutrophil activation and traumaR01GM060475 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI JUNGER, WOLFGANG G · 2001 to 2016
$3.8M
Purinergic regulation of T cellsR01GM051477 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI JUNGER, WOLFGANG G · 2003 to 2016
$2.5M
Role of purinergic signaling in pediatric multi-organ failureR01HD098363 · NICHD · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI JUNGER, WOLFGANG G · 2019 to 2023
$2.0M
Autocrine regulation of neutrophil chemotaxisR01GM116162 · NIGMS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI JUNGER, WOLFGANG G · 2015 to 2018
$1.6M
Purinergic receptors in inflammationR01AI080582 · NIAID · BETH ISRAEL DEACONESS MEDICAL CENTER · PI JUNGER, WOLFGANG G · 2009 to 2012
$1.4M
Harvard Trauma Inflammation Training ProgramT32GM103702 · NIGMS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI JUNGER, WOLFGANG G · 2013 to 2017
$922k
Autocrine control of neutrophil chemotaxisR01AI072287 · NIAID · BETH ISRAEL DEACONESS MEDICAL CENTER · PI JUNGER, WOLFGANG G · 2009 to 2010
$766k
HYPERTONIC SALINE AND IMMUNE FUNCTIONR29GM051477 · NIGMS · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI JUNGER, WOLFGANG G · 1996 to 2000
$116k
NIAID NIH HHS R01 AI072287NIAID NIH HHS R01 AI080582NICHD NIH HHS R01 HD098363NIGMS NIH HHS R01 GM051477NIGMS NIH HHS R01 GM060475NIGMS NIH HHS R01 GM116162NIGMS NIH HHS R29 GM051477NIGMS NIH HHS T32 GM103702
6 · The paper itself

Abstract

Bacterial infections and sepsis are leading causes of morbidity and mortality in critically ill patients. Currently, there are no effective treatments available to improve clinical outcome in sepsis. Here, we elucidated a mechanism by which Escherichia coli (E. coli) bacteria impair neutrophil (PMN) chemotaxis and we studied whether this mechanism can be therapeutically targeted to improve chemotaxis and antimicrobial host defense. PMNs detect bacteria with formyl peptide receptors (FPR). FPR stimulation triggers mitochondrial ATP production and release. Autocrine stimulation of purinergic receptors exerts excitatory and inhibitory downstream signals that induce cell polarization and cell shape changes needed for chemotaxis. Here we show that the bacterial cell wall product LPS dose-dependently impairs PMN chemotaxis. Exposure of human PMNs to LPS triggered excessive mitochondrial ATP production and disorganized intracellular trafficking of mitochondria, resulting in global ATP release that disrupted purinergic signaling, cell polarization, and chemotaxis. In mice infected i.p. with E. coli, LPS treatment increased the spread of bacteria at the infection site and throughout the systemic circulation. Removal of excessive systemic ATP with apyrase improved chemotaxis of LPS-treated human PMNs in vitro and enhanced the clearance of E. coli in infected and LPS-treated mice. We conclude that systemic ATP accumulation in response to LPS is a potential therapeutic target to restore PMN chemotaxis and to boost the antimicrobial host immune defense in sepsis.

Indexed as

AdenosineAdenosine MonophosphateAdenosine TriphosphateAnimalsApyraseBiomarkersChemotaxis, LeukocyteDisease Models, AnimalEscherichia coliEscherichia coli InfectionsHost-Pathogen InteractionsHumansIntracellular SpaceLipopolysaccharidesMiceMitochondriaAdenosineAdenosine MonophosphateAdenosine TriphosphateApyraseBiomarkersLipopolysaccharidesapyraseATP releasebacterial clearanceendotoxinpurinergic signaling

Identifiers

PMID31392789
PMCPMC6883117
OpenAlexW2969152882

What OpenQuestion holds

Textmetadata
LicenceTDM
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.