Evidence map›Paper›PMID 34687607›Full record

ArticleImmunity2021

Nitric oxide controls proliferation of Leishmania major by inhibiting the recruitment of permissive host cells.

Pauline Formaglio, Mohamad Alabdullah, Anastasios Siokis, Juliane Handschuh, Ina Sauerland, Yan Fu, Anna Krone, Patricia Gintschel, Juliane Stettin, Sandrina Heyde and 16 more

Open access · hybridAbstract read
In one paragraph

Article in Immunity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

29 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
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  12. Unleashing the immune modulatory potential ofFrontiers in molecular biosciences · 2025
    Article
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  19. Leishmanicidal Activity of Guanidine Derivatives againstTropical medicine and infectious disease · 2023
    Article
  20. 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

26 authors at 7 institutions in 3 countries.

Pauline FormaglioInstitute of Molecular and Clinical Immunology, Health Campus Immunology Infectiology and Inflammation (GC-I(3)), Otto-von-Guericke-University, Magdeburg 39120, Germany. Electronic address: pauline.formaglio@pasteur.fr.
Mohamad AlabdullahInstitute of Molecular and Clinical Immunology, Health Campus Immunology Infectiology and Inflammation (GC-I(3)), Otto-von-Guericke-University, Magdeburg 39120, Germany.
Anastasios SiokisDepartment of Systems Immunology and Braunschweig Integrated Centre of Systems Biology, Helmholtz Centre for Infection Research, Braunschweig 38124, Germany.
Juliane HandschuhInstitute of Molecular and Clinical Immunology, Health Campus Immunology Infectiology and Inflammation (GC-I(3)), Otto-von-Guericke-University, Magdeburg 39120, Germany.
Ina SauerlandInstitute of Molecular and Clinical Immunology, Health Campus Immunology Infectiology and Inflammation (GC-I(3)), Otto-von-Guericke-University, Magdeburg 39120, Germany.
Yan FuInstitute of Molecular and Clinical Immunology, Health Campus Immunology Infectiology and Inflammation (GC-I(3)), Otto-von-Guericke-University, Magdeburg 39120, Germany.
Anna KroneInstitute of Molecular and Clinical Immunology, Health Campus Immunology Infectiology and Inflammation (GC-I(3)), Otto-von-Guericke-University, Magdeburg 39120, Germany.
Patricia GintschelInstitute of Molecular and Clinical Immunology, Health Campus Immunology Infectiology and Inflammation (GC-I(3)), Otto-von-Guericke-University, Magdeburg 39120, Germany.
Juliane StettinInstitute of Molecular and Clinical Immunology, Health Campus Immunology Infectiology and Inflammation (GC-I(3)), Otto-von-Guericke-University, Magdeburg 39120, Germany.
Sandrina HeydeInstitute of Molecular and Clinical Immunology, Health Campus Immunology Infectiology and Inflammation (GC-I(3)), Otto-von-Guericke-University, Magdeburg 39120, Germany.
Juliane MohrInstitute of Molecular and Clinical Immunology, Health Campus Immunology Infectiology and Inflammation (GC-I(3)), Otto-von-Guericke-University, Magdeburg 39120, Germany.
Lars PhilipsenInstitute of Molecular and Clinical Immunology, Health Campus Immunology Infectiology and Inflammation (GC-I(3)), Otto-von-Guericke-University, Magdeburg 39120, Germany.
Anja SchröderExperimental Orthopedics, Health Campus Immunology Infectiology and Inflammation (GC-I(3)), Otto von Guericke University, Magdeburg 39120, Germany.
Philippe A RobertDepartment of Systems Immunology and Braunschweig Integrated Centre of Systems Biology, Helmholtz Centre for Infection Research, Braunschweig 38124, Germany; Department of Immunology, University of Oslo, Oslo 0372, Norway.
Gang ZhaoDepartment of Systems Immunology and Braunschweig Integrated Centre of Systems Biology, Helmholtz Centre for Infection Research, Braunschweig 38124, Germany.
Sahamoddin KhailaieDepartment of Systems Immunology and Braunschweig Integrated Centre of Systems Biology, Helmholtz Centre for Infection Research, Braunschweig 38124, Germany.
Anne DudeckInstitute of Molecular and Clinical Immunology, Health Campus Immunology Infectiology and Inflammation (GC-I(3)), Otto-von-Guericke-University, Magdeburg 39120, Germany.
Jessica BertrandExperimental Orthopedics, Health Campus Immunology Infectiology and Inflammation (GC-I(3)), Otto von Guericke University, Magdeburg 39120, Germany.
Gerald F SpäthMolecular Parasitology and Signalling Unit, Institut Pasteur, Paris 75015, France.
Sascha KahlfußInstitute of Molecular and Clinical Immunology, Health Campus Immunology Infectiology and Inflammation (GC-I(3)), Otto-von-Guericke-University, Magdeburg 39120, Germany.
Philippe BoussoDynamics of Immune Responses Unit, Institut Pasteur, INSERM U1223, Paris 75015, France.
Burkhart SchravenInstitute of Molecular and Clinical Immunology, Health Campus Immunology Infectiology and Inflammation (GC-I(3)), Otto-von-Guericke-University, Magdeburg 39120, Germany.
Jochen HuehnDepartment Experimental Immunology, Helmholtz Centre for Infection Research, 38124 Braunschweig, Germany; Cluster of Excellence RESIST (EXC 2155), Hannover Medical School, Hannover 30625, Germany.
Sebastian BinderDepartment of Systems Immunology and Braunschweig Integrated Centre of Systems Biology, Helmholtz Centre for Infection Research, Braunschweig 38124, Germany.
Michael Meyer-HermannDepartment of Systems Immunology and Braunschweig Integrated Centre of Systems Biology, Helmholtz Centre for Infection Research, Braunschweig 38124, Germany; Institute of Biochemistry, Biotechnology and Bioinformatics, Technische Universität Braunschweig, Braunschweig 38106, Germany.
Andreas J MüllerInstitute of Molecular and Clinical Immunology, Health Campus Immunology Infectiology and Inflammation (GC-I(3)), Otto-von-Guericke-University, Magdeburg 39120, Germany; Intravital Microscopy of Infection and Immunity, Helmholtz Centre for Infection Research, Braunschweig 38124, Germany. Electronic address: andreas.mueller@med.ovgu.de.
Otto-von-Guericke-Universität Magdeburg · DEHelmholtz Centre for Infection Research · DEBiology of Infection · FRInserm · FRInstitut Pasteur · FRMedizinische Hochschule Hannover · DEUniversity of Oslo · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nitric oxide (NO) is an important antimicrobial effector but also prevents unnecessary tissue damage by shutting down the recruitment of monocyte-derived phagocytes. Intracellular pathogens such as Leishmania major can hijack these cells as a niche for replication. Thus, NO might exert containment by restricting the availability of the cellular niche required for efficient pathogen proliferation. However, such indirect modes of action remain to be established. By combining mathematical modeling with intravital 2-photon biosensors of pathogen viability and proliferation, we show that low L. major proliferation results not from direct NO impact on the pathogen but from reduced availability of proliferation-permissive host cells. Although inhibiting NO production increases recruitment of these cells, and thus pathogen proliferation, blocking cell recruitment uncouples the NO effect from pathogen proliferation. Therefore, NO fulfills two distinct functions for L. major containment: permitting direct killing and restricting the supply of proliferation-permissive host cells.

Indexed as

AnimalsCell Growth ProcessesCell MovementCell ProliferationDisease Models, AnimalHost-Pathogen InteractionsHumansIntravital MicroscopyLeishmania majorLeishmaniasisMacrophagesMiceMice, Inbred C57BLModels, TheoreticalNitric OxideNitric Oxide2-photon microscopybiosensorinflammationiNOSintracellular pathogenLeishmaniamonocytenitric oxidephagocyte

Identifiers

PMID34687607
PMCPMC8691385
OpenAlexW3209036622

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.