Evidence map›Paper›PMID 36341426›Full record

ReviewFrontiers in immunology2022

Role of metabolic reprogramming in pro-inflammatory cytokine secretion from LPS or silica-activated macrophages.

Antonella Marrocco, Luis A Ortiz

Abstract readReview
In one paragraph

Review in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.

0numbers the graph read from it
0cells of the map it votes in
87citing 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

87 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Mechanisms Involved in Pathological Succinate-Mediated Signaling.International journal of molecular sciences · 2026
    Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Epigenetic programming of macrophages across inflammatory and malignant diseases.Naunyn-Schmiedeberg's archives of pharmacology · 2026
    Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. Article

27 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

2 authors.

Antonella MarroccoDepartment of Environmental and Occupational Health, School of Public Health, University of Pittsburgh, Pittsburgh, PA, United States.
Luis A OrtizDepartment of Environmental and Occupational Health, School of Public Health, University of Pittsburgh, Pittsburgh, PA, United States.

Funding

RV/PA Recoupling by Bone Marrow Derived Mesenchymal Stem CellsR01HL114795 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI ORTIZ, LUIS ALBERTO · 2012 to 2016
$3.4M
Mesenchymal stem cell secretome in lung fibrosis: mitochondria and RNA shuttleR01HL110344 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI ORTIZ, LUIS ALBERTO · 2013 to 2016
$1.6M
NHLBI NIH HHS R01 HL110344NHLBI NIH HHS R01 HL114795
6 · The paper itself

Abstract

In the lungs, macrophages constitute the first line of defense against pathogens and foreign bodies and play a fundamental role in maintaining tissue homeostasis. Activated macrophages show altered immunometabolism and metabolic changes governing immune effector mechanisms, such as cytokine secretion characterizing their classic (M1) or alternative (M2) activation. Lipopolysaccharide (LPS)-stimulated macrophages demonstrate enhanced glycolysis, blocked succinate dehydrogenase (SDH), and increased secretion of interleukin-1 beta (IL-1β) and tumor necrosis factor-alpha (TNF-α). Glycolysis suppression using 2 deoxyglucose in LPS-stimulated macrophages inhibits IL-1β secretion, but not TNF-α, indicating metabolic pathway specificity that determines cytokine production. In contrast to LPS, the nature of the immunometabolic responses induced by non-organic particles, such as silica, in macrophages, its contribution to cytokine specification, and disease pathogenesis are not well understood. Silica-stimulated macrophages activate pattern recognition receptors (PRRs) and NLRP3 inflammasome and release IL-1β, TNF-α, and interferons, which are the key mediators of silicosis pathogenesis. In contrast to bacteria, silica particles cannot be degraded, and the persistent macrophage activation results in an increased NADPH oxidase (Phox) activation and mitochondrial reactive oxygen species (ROS) production, ultimately leading to macrophage death and release of silica particles that perpetuate inflammation. In this manuscript, we reviewed the effects of silica on macrophage mitochondrial respiration and central carbon metabolism determining cytokine specification responsible for the sustained inflammatory responses in the lungs.

Indexed as

LipopolysaccharidesSilicon DioxideCytokinesMacrophage ActivationMacrophagesTumor Necrosis Factor-alphaCytokinesLipopolysaccharidesSilicon DioxideTumor Necrosis Factor-alphacomplex IIelectron transport chainM1 macrophagesmacrophage immunometabolismmacrophage metabolic adaptationmitochondriarespirable crystalline silica

Identifiers

PMID36341426
PMCPMC9633986

What OpenQuestion holds

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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.