Evidence map›Paper›PMID 40479071›Full record

ArticleScience advances2025

Chemokines kill bacteria without triggering antimicrobial resistance by binding anionic phospholipids.

Sergio M Pontejo, Sophia Martinez, Allison Zhao, Kevin Barnes, Jaime de Anda, Haleh Alimohamadi, Ernest Y Lee, Acacia F Dishman, Brian F Volkman, Gerard C L Wong and 3 more

Abstract read
In one paragraph

Article in Science advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. iScience · 2025
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors.

Sergio M PontejoLaboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.ORCID 0000-0002-7756-9831
Sophia MartinezLaboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.ORCID 0009-0008-3078-3487
Allison ZhaoLaboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.ORCID 0009-0009-0761-9205
Kevin BarnesStructural Biology Section, Research Technologies Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.ORCID 0009-0006-7888-7512
Jaime de AndaDepartment of Bioengineering, University of California, Los Angeles, Los Angeles, CA 90095, USA.ORCID 0000-0003-2129-0775
Haleh AlimohamadiDepartment of Bioengineering, University of California, Los Angeles, Los Angeles, CA 90095, USA.ORCID 0000-0001-6576-2426
Ernest Y LeeDepartment of Bioengineering, University of California, Los Angeles, Los Angeles, CA 90095, USA.ORCID 0000-0001-5144-2552
Acacia F DishmanDepartment of Biochemistry, Medical College of Wisconsin, Milwaukee, WI 53226, USA.
Brian F VolkmanDepartment of Biochemistry, Medical College of Wisconsin, Milwaukee, WI 53226, USA.ORCID 0000-0002-6681-5179
Gerard C L WongDepartment of Bioengineering, University of California, Los Angeles, Los Angeles, CA 90095, USA.ORCID 0000-0003-0893-6383
David N GarbocziStructural Biology Section, Research Technologies Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.ORCID 0000-0002-2545-854X
Angela BallesterosSection on Sensory Physiology and Biophysics, National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, MD 20892, USA.ORCID 0000-0001-5796-6875
Philip M MurphyLaboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.ORCID 0000-0002-1080-8201

Funding

Structural Basis for Chemokine FunctionR37AI058072 · NIAID · MEDICAL COLLEGE OF WISCONSIN · PI Brian F Volkman · 2020 to 2026
$2.8M
NIAID NIH HHS R37 AI058072
6 · The paper itself

Abstract

Classically, chemokines coordinate leukocyte trafficking; however, many chemokines also have direct antibacterial activity. The bacterial killing mechanism of chemokines and the biochemical properties that define which members of the chemokine superfamily are antimicrobial remain poorly understood. We report that the antimicrobial activity of chemokines is defined by their ability to bind phosphatidylglycerol and cardiolipin, two anionic phospholipids commonly found in the bacterial plasma membrane. We show that only chemokines able to bind these two phospholipids kill bacteria and that they exert rapid bacteriostatic and bactericidal effects with a higher potency than the antimicrobial peptide β-defensin 3. Both biochemical and genetic interference with the chemokine-cardiolipin interaction impaired microbial growth arrest, bacterial killing, and membrane disruption by chemokines. Moreover, unlike conventional antibiotics,

Indexed as

Anti-Bacterial AgentsBacteriaChemokinesDrug Resistance, BacterialEscherichia coliPhospholipidsCardiolipinsCell MembraneHumansMicrobial Sensitivity TestsPhosphatidylglycerolsProtein BindingAnti-Bacterial AgentsCardiolipinsChemokinesPhosphatidylglycerolsPhospholipids

Identifiers

PMID40479071
PMCPMC12143392

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.