Evidence map›Paper›PMID 32547553›Full record

ReviewFrontiers in immunology2020

The Metabolic Basis of Immune Dysfunction Following Sepsis and Trauma.

Margaret A McBride, Allison M Owen, Cody L Stothers, Antonio Hernandez, Liming Luan, Katherine R Burelbach, Tazeen K Patil, Julia K Bohannon, Edward R Sherwood, Naeem K Patil

Abstract readReview
In one paragraph

Review in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed, 1 pooled it
–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

70 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Sepsis and the immunometabolic inflammatory response.npj metabolic health and disease · 2026
    Review
  6. Metabolic adaptations rewire CD4Nature immunology · 2026
    Article
  7. Review
  8. Review
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  10. Article
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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

10 authors.

Margaret A McBrideDepartment of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, TN, United States.
Allison M OwenDepartment of Anesthesiology, Vanderbilt University Medical Center, Nashville, TN, United States.
Cody L StothersDepartment of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, TN, United States.
Antonio HernandezDepartment of Anesthesiology, Vanderbilt University Medical Center, Nashville, TN, United States.
Liming LuanDepartment of Anesthesiology, Vanderbilt University Medical Center, Nashville, TN, United States.
Katherine R BurelbachDepartment of Anesthesiology, Vanderbilt University Medical Center, Nashville, TN, United States.
Tazeen K PatilDepartment of Anesthesiology, Vanderbilt University Medical Center, Nashville, TN, United States.
Julia K BohannonDepartment of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, TN, United States.
Edward R SherwoodDepartment of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, TN, United States.
Naeem K PatilDepartment of Anesthesiology, Vanderbilt University Medical Center, Nashville, TN, United States.

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007347 · NIGMS · VANDERBILT UNIVERSITY · PI WILLIAMS, CHRISTOPHER S. · 1985 to 2023
$26.3M
Medical Scientist Training ProgramT32GM152284 · NIGMS · VANDERBILT UNIVERSITY · PI Christopher S. Williams · 2024 to 2026
$4.8M
Training Innate Immunity: A new approach to the treatment of SepsisR01GM119197 · NIGMS · EAST TENNESSEE STATE UNIVERSITY · PI SHERWOOD, EDWARD R, WILLIAMS, DAVID L. · 2016 to 2024
$4.6M
TIPS: Training in Perioperative ScienceT32GM108554 · NIGMS · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Eric J Delpire · 2014 to 2026
$3.7M
Macrophage mitochodrial reprogramming and innate immune memoryR01AI151210 · NIAID · VANDERBILT UNIVERSITY MEDICAL CENTER · PI SHERWOOD, EDWARD R · 2020 to 2024
$2.1M
Enhancing Resistance to Infection after Burn Injury with TLR AgonistsR01GM121711 · NIGMS · VANDERBILT UNIVERSITY MEDICAL CENTER · PI BOHANNON, JULIA K. · 2017 to 2021
$1.6M
Augmentation of Innate Anti-Microbial Immunity by TLR4 AgonistsR01GM104306 · NIGMS · VANDERBILT UNIVERSITY MEDICAL CENTER · PI ENKHBAATAR, PERENLEI, SHERWOOD, EDWARD R · 2013 to 2016
$1.2M
Enhancement of Innate Anti-Microbial Immunity Using Novel Synthetic TLR4 AgonistsK08GM123345 · NIGMS · VANDERBILT UNIVERSITY MEDICAL CENTER · PI HERNANDEZ, ANTONIO · 2017 to 2020
$699k
NIAID NIH HHS R01 AI151210NIGMS NIH HHS K08 GM123345NIGMS NIH HHS R01 GM104306NIGMS NIH HHS R01 GM119197NIGMS NIH HHS R01 GM121711NIGMS NIH HHS T32 GM007347NIGMS NIH HHS T32 GM108554NIGMS NIH HHS T32 GM152284
6 · The paper itself

Abstract

Critically ill, severely injured and high-risk surgical patients are vulnerable to secondary infections during hospitalization and after hospital discharge. Studies show that the mitochondrial function and oxidative metabolism of monocytes and macrophages are impaired during sepsis. Alternatively, treatment with microbe-derived ligands, such as monophosphoryl lipid A (MPLA), peptidoglycan, or β-glucan, that interact with toll-like receptors and other pattern recognition receptors on leukocytes induces a state of innate immune memory that confers broad-spectrum resistance to infection with common hospital-acquired pathogens. Priming of macrophages with MPLA, CPG oligodeoxynucleotides (CpG ODN), or β-glucan induces a macrophage metabolic phenotype characterized by mitochondrial biogenesis and increased oxidative metabolism in parallel with increased glycolysis, cell size and granularity, augmented phagocytosis, heightened respiratory burst functions, and more effective killing of microbes. The mitochondrion is a bioenergetic organelle that not only contributes to energy supply, biosynthesis, and cellular redox functions but serves as a platform for regulating innate immunological functions such as production of reactive oxygen species (ROS) and regulatory intermediates. This review will define current knowledge of leukocyte metabolic dysfunction during and after sepsis and trauma. We will further discuss therapeutic strategies that target leukocyte mitochondrial function and might have value in preventing or reversing sepsis- and trauma-induced immune dysfunction.

Indexed as

AnimalsCellular ReprogrammingHumansImmunity, InnateInfectionsLeukocytesMitochondriaOxidative StressSepsisWounds and Injuriesinfectionmetabolic reprogrammingmitochondriasepsistrained immunitytrauma

Identifiers

PMID32547553
PMCPMC7273750

What OpenQuestion holds

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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.