Evidence map›Paper›PMID 41387444›Full record

ArticleNature communications2025

G-CSF/NAMPT signaling drives neutrophil dysfunction and enhances bacterial infection susceptibility in cancer patients.

Ekaterina Pylaeva, Lea Tollrian, Jana Riedesel, Olga Shevchuk, Ilona Thiel, Irem Ozel, Nastassia Kabankova, Hannah Voß, Bente Siebels, Hartmut Schlüter and 9 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Review
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

19 authors.

Ekaterina PylaevaDepartment of Otorhinolaryngology, Head and Neck Surgery, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.ORCID http://orcid.org/0000-0002-3941-9664
Lea TollrianDepartment of Otorhinolaryngology, Head and Neck Surgery, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Jana RiedeselDepartment of Otorhinolaryngology, Head and Neck Surgery, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Olga ShevchukDepartment of Immunodynamics, Institute for Experimental Immunology and Imaging, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.ORCID http://orcid.org/0000-0003-1150-7344
Ilona ThielDepartment of Otorhinolaryngology, Head and Neck Surgery, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Irem OzelDepartment of Otorhinolaryngology, Head and Neck Surgery, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.ORCID http://orcid.org/0000-0002-7007-9928
Nastassia KabankovaDepartment of Otorhinolaryngology, Head and Neck Surgery, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.ORCID http://orcid.org/0000-0003-1506-4923
Hannah VoßDepartment of Immunodynamics, Institute for Experimental Immunology and Imaging, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Bente SiebelsSection Mass Spectrometry and Proteomics, Center for Diagnostics, University Medical Center Hamburg-Eppendorf (UKE), Hamburg, Germany.
Hartmut SchlüterSection Mass Spectrometry and Proteomics, Center for Diagnostics, University Medical Center Hamburg-Eppendorf (UKE), Hamburg, Germany.ORCID http://orcid.org/0000-0002-9358-7036
Corinna HaistDepartment of Otorhinolaryngology and Head/Neck Surgery, Heinrich Heine University, Düsseldorf, Germany.
Helmut HanenbergDepartment of Otorhinolaryngology and Head/Neck Surgery, Heinrich Heine University, Düsseldorf, Germany.
Stefan MattheisDepartment of Otorhinolaryngology, Head and Neck Surgery, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Cornelius KürtenDepartment of Otorhinolaryngology, Head and Neck Surgery, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Markus SperandioInstitute of Cardiovascular Physiology and Pathophysiology, Biomedical Center, Ludwig Maximilian University of Munich, Munich, Germany.ORCID http://orcid.org/0000-0002-7689-3613
Jan KehrmannInstitute of Medical Microbiology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Daniel Robert EngelDepartment of Immunodynamics, Institute for Experimental Immunology and Imaging, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Stephan LangDepartment of Otorhinolaryngology, Head and Neck Surgery, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Jadwiga JablonskaDepartment of Otorhinolaryngology, Head and Neck Surgery, University Hospital Essen, University of Duisburg-Essen, Essen, Germany. Jadwiga.Jablonska@uk-essen.de.ORCID http://orcid.org/0000-0003-1490-2542

Funding

Deutsche Forschungsgemeinschaft (German Research Foundation) DFG/ JA 2461/2-1Deutsche Forschungsgemeinschaft (German Research Foundation) DFG/ JA 2461/7-1Deutsche Forschungsgemeinschaft (German Research Foundation) TR332 A5Deutsche Krebshilfe (German Cancer Aid) 111647
6 · The paper itself

Abstract

Despite advancements in cancer therapies, bacterial complications remain a major challenge, delaying treatment and worsening outcomes. While immunosuppressive therapies and prolonged hospitalizations contribute, they do not fully explain the elevated infection risk in cancer patients. Here we show that tumors producing high levels of granulocyte colony-stimulating factor (G-CSF) promote the persistence of Gram-negative pathogens in head and neck squamous cell carcinoma due to neutrophil reprogramming. Mechanistically, we identify tumor-driven activation of the G-CSF / nicotinamide phosphoribosyltransferase (NAMPT) signaling axis in neutrophil progenitors, resulting in impaired antibacterial functions, such as phagocytosis and neutrophil extracellular traps formation, and development of tissue-damaging neutrophil subsets. This disrupts lung tissue integrity and facilitates bacterial persistence. Importantly, targeting the G-CSF/NAMPT pathway prevents the generation of dysfunctional neutrophils and improves bacterial clearance in vivo. Our findings reveal tumor-induced, NAMPT-dependent neutrophil reprogramming as a central driver of compromised antimicrobial defenses in cancer. Therapeutic strategies aimed at modulating G-CSF/NAMPT signaling could enhance infection control and survival for cancer patients.

Indexed as

Bacterial InfectionsNeutrophilsSignal TransductionAnimalsCell DifferentiationCell Line, TumorCytokinesDisease SusceptibilityEnzyme ActivationFemaleGranulocyte Colony-Stimulating FactorHead and Neck NeoplasmsHumansMaleMiceMice, Inbred C57BLCytokinesGranulocyte Colony-Stimulating FactorNicotinamide Phosphoribosyltransferasenicotinamide phosphoribosyltransferase, human

Identifiers

PMID41387444
PMCPMC12705696

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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.