Evidence map›Paper›PMID 27671632›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2016

Exogenous remodeling of lung resident macrophages protects against infectious consequences of bone marrow-suppressive chemotherapy.

Akinobu Kamei, Geli Gao, Geoffrey Neale, Lip Nam Loh, Peter Vogel, Paul G Thomas, Elaine I Tuomanen, Peter J Murray

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

12 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Molecular mechanisms that govern infection and antifungal resistance in Mucorales.Microbiology and molecular biology reviews : MMBR · 2024
    Review
  3. Article
  4. Article
  5. Article
  6. Transcriptome profiling in swine macrophages infected with African swine fever virus at single-cell resolution.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
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

8 authors at 1 institution in 2 countries.

Akinobu KameiDepartment of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, TN 38105; Department of Pediatrics, Keio University School of Medicine, Tokyo 160-8582, Japan; peter.murray@stjude.org akinobu.kamei@stjude.org.
Geli GaoDepartment of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, TN 38105.
Geoffrey NealeHartwell Center for Bioinformatics and Biotechnology, St. Jude Children's Research Hospital, Memphis, TN 38105.
Lip Nam LohDepartment of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, TN 38105.
Peter VogelDepartment of Pathology, St. Jude Children's Research Hospital, Memphis, TN 38105.
Paul G ThomasDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105.
Elaine I TuomanenDepartment of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, TN 38105.
Peter J MurrayDepartment of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, TN 38105; Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105 peter.murray@stjude.org akinobu.kamei@stjude.org.
St. Jude Children's Research Hospital · US

Funding

Viral Vector Technology (VVTSR)P30CA021765 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI CHARLES ROBERTS · 1985 to 2026
$166.9M
PNEUMOCOCCAL CELL WALL IN MENINGITISR01AI027913 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI TUOMANEN, ELAINE I · 1989 to 2015
$5.2M
NCI NIH HHS P30 CA021765NIAID NIH HHS HHSN272201400006CNIAID NIH HHS R01 AI027913
6 · The paper itself

Abstract

Infection is the single greatest threat to survival during cancer chemotherapy because of depletion of bone marrow-derived immune cells. Phagocytes, especially neutrophils, are key effectors in immunity to extracellular pathogens, which has limited the development of new approaches to protect patients with cancer and chemotherapy-induced neutropenia. Using a model of vaccine-induced protection against lethal Pseudomonas aeruginosa pneumonia in the setting of chemotherapy-induced neutropenia, we found a population of resident lung macrophages in the immunized lung that mediated protection in the absence of neutrophils, bone marrow-derived monocytes, or antibodies. These vaccine-induced macrophages (ViMs) expanded after immunization, locally proliferated, and were closely related to alveolar macrophages (AMs) by surface phenotype and gene expression profiles. By contrast to AMs, numbers of ViMs were stable through chemotherapy, showed enhanced phagocytic activity, and prolonged survival of neutropenic mice from lethal P. aeruginosa pneumonia upon intratracheal adoptive transfer. Thus, induction of ViMs by tissue macrophage remodeling may become a framework for new strategies to activate immune-mediated reserves against infection in immunocompromised hosts.

Indexed as

AnimalsAntineoplastic AgentsBiomarkersBone MarrowCell CycleDisease Models, AnimalDisease ResistanceGene Expression ProfilingHost-Pathogen InteractionsImmunophenotypingMacrophages, AlveolarMiceMice, KnockoutNeutropeniaPhagocytosisPseudomonas aeruginosaAntineoplastic AgentsBiomarkersPseudomonas VaccineschemotherapymacrophageneutropeniaPseudomonas aeruginosa pneumoniavaccine

Identifiers

PMID27671632
PMCPMC5068317
OpenAlexW2526634236

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.