Evidence map›Paper›PMID 31786568›Full record

ReviewJournal of innate immunity2020

Role of Metabolic Reprogramming in Pulmonary Innate Immunity and Its Impact on Lung Diseases.

Charalambos Michaeloudes, Pankaj K Bhavsar, Sharon Mumby, Bingling Xu, Christopher Kim Ming Hui, Kian Fan Chung, Ian M Adcock

Open access · goldAbstract readReview
In one paragraph

Review in Journal of innate immunity, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
7.7field-weighted citation impact, top 2% 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

70 citing papers in PubMed, 108 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Review
  5. Trained immunity in respiratory diseases: Mechanisms of action and intervention strategies.Chinese medical journal pulmonary and critical care medicine · 2026
    Review
  6. Asthma endotypes and theratypes.Chinese medical journal pulmonary and critical care medicine · 2026
    Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. Metabolomic profiling ofmSystems · 2025
    Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review

10 more citing papers are in PubMed but not listed here.

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

7 authors at 3 institutions in 3 countries.

Charalambos MichaeloudesExperimental Studies and Cell and Molecular Biology, Airway Disease Section, National Heart and Lung Institute, Imperial College London and Biomedical Research Unit, Royal Brompton Hospital, London, United Kingdom, c.michaeloudes04@imperial.ac.uk.
Pankaj K BhavsarExperimental Studies and Cell and Molecular Biology, Airway Disease Section, National Heart and Lung Institute, Imperial College London and Biomedical Research Unit, Royal Brompton Hospital, London, United Kingdom.
Sharon MumbyExperimental Studies and Cell and Molecular Biology, Airway Disease Section, National Heart and Lung Institute, Imperial College London and Biomedical Research Unit, Royal Brompton Hospital, London, United Kingdom.
Bingling XuRespiratory and Critical Care Medicine, The University of Hong Kong-Shenzhen Hospital, Shenzhen, China.
Christopher Kim Ming HuiRespiratory and Critical Care Medicine, The University of Hong Kong-Shenzhen Hospital, Shenzhen, China.
Kian Fan ChungExperimental Studies and Cell and Molecular Biology, Airway Disease Section, National Heart and Lung Institute, Imperial College London and Biomedical Research Unit, Royal Brompton Hospital, London, United Kingdom.
Ian M AdcockExperimental Studies and Cell and Molecular Biology, Airway Disease Section, National Heart and Lung Institute, Imperial College London and Biomedical Research Unit, Royal Brompton Hospital, London, United Kingdom.
Imperial College London · GBRoyal Brompton Hospital · GBUniversity of Hong Kong · HK

Funding

The Dunhill Medical Trust R368/0714
6 · The paper itself

Abstract

Lung innate immunity is the first line of defence against inhaled allergens, pathogens and environmental pollutants. Cellular metabolism plays a key role in innate immunity. Catabolic pathways, including glycolysis and fatty acid oxidation (FAO), are interconnected with biosynthetic and redox pathways. Innate immune cell activation and differentiation trigger extensive metabolic changes that are required to support their function. Pro-inflammatory polarisation of macrophages and activation of dendritic cells, mast cells and neutrophils are associated with increased glycolysis and a shift towards the pentose phosphate pathway and fatty acid synthesis. These changes provide the macromolecules required for proliferation and inflammatory mediator production and reactive oxygen species for anti-microbial effects. Conversely, anti-inflammatory macrophages use primarily FAO and oxidative phosphorylation to ensure efficient energy production and redox balance required for prolonged survival. Deregulation of metabolic reprogramming in lung diseases, such as asthma and chronic obstructive pulmonary disease, may contribute to impaired innate immune cell function. Understanding how innate immune cell metabolism is altered in lung disease may lead to identification of new therapeutic targets. This is important as drugs targeting a number of metabolic pathways are already in clinical development for the treatment of other diseases such as cancer.

Indexed as

AnimalsCellular ReprogrammingGlycolysisHumansImmunity, InnateLungLung DiseasesMacrophagesOxidative PhosphorylationPentose Phosphate PathwayAsthmaBiosynthesisChronic obstructive pulmonary diseaseGlycolysisMitochondria

Identifiers

PMID31786568
PMCPMC6959099
OpenAlexW2989848490

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.