Evidence map›Paper›PMID 28154172›Full record

ArticleThe Journal of biological chemistry2017

Metabolic Alterations Contribute to Enhanced Inflammatory Cytokine Production in Irgm1-deficient Macrophages.

Elyse A Schmidt, Brian E Fee, Stanley C Henry, Amanda G Nichols, Mari L Shinohara, Jeffrey C Rathmell, Nancie J MacIver, Jörn Coers, Olga R Ilkayeva, Timothy R Koves and 1 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

21 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Irgm1 Restrains CD8European journal of immunology · 2026
    Article
  3. Macrophages From Latently Infected Mice Have Trained Immunity to HSV-1.Investigative ophthalmology & visual science · 2026
    Article
  4. Article
  5. Autophagy and Bacterial infections.Autophagy reports · 2025
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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

11 authors at 6 institutions in 1 country.

Elyse A SchmidtFrom the Departments of Molecular Genetics and Microbiology.
Brian E Feethe Geriatric Research, Education, and Clinical Center, Durham Veterans Affairs Health Care System, Durham, North Carolina 27705, and.
Stanley C Henrythe Geriatric Research, Education, and Clinical Center, Durham Veterans Affairs Health Care System, Durham, North Carolina 27705, and.
Amanda G Nicholsthe Department of Pediatrics, Division of Pediatric Endocrinology and Diabetes.
Mari L ShinoharaFrom the Departments of Molecular Genetics and Microbiology.
Jeffrey C Rathmellthe Department of Pathology, Microbiology, and Immunology, Vanderbilt Center for Immunobiology, Vanderbilt University, Nashville, Tennessee 37232.
Nancie J MacIverthe Department of Pediatrics, Division of Pediatric Endocrinology and Diabetes.
Jörn CoersFrom the Departments of Molecular Genetics and Microbiology.
Olga R Ilkayevathe Duke Molecular Physiology Institute, and.
Timothy R Kovesthe Duke Molecular Physiology Institute, and.
Gregory A TaylorFrom the Departments of Molecular Genetics and Microbiology, gregory.taylor@duke.edu.
Duke Medical Center · USDuke University · USDuke University Hospital · USDurham VA Health Care System · USGeriatric Research Education and Clinical Center · USVanderbilt University · US

Funding

Regional Biocontainment Laboratory (RBL)UC6AI058607 · NIAID · DUKE UNIVERSITY · PI WILLIAMS, R SANDERS · 2003 to 2005
$16.3M
Role of osteopontin in innate immunity during infections and inflammationR01AI088100 · NIAID · DUKE UNIVERSITY · PI SHINOHARA, MARI L. · 2011 to 2021
$4.3M
IRGM-driven host responses to Chlamydia trachomatis infectionsR01AI103197 · NIAID · DUKE UNIVERSITY · PI COERS, JOERN · 2013 to 2023
$4.2M
Regulation of IFN-g-induced Innate Immunity by LRG-47R01AI057831 · NIAID · DUKE UNIVERSITY · PI TAYLOR, GREGORY A · 2004 to 2013
$3.1M
Mechanisms of T cell inflammation in obesity-induced type 2 diabetesR01DK106090 · NIDDK · DUKE UNIVERSITY · PI MACIVER, NANCIE · 2015 to 2019
$1.8M
Interferon-inducible cell-intrinsic host defense against Chlamydia trachomatisR37AI103197 · NIAID · DUKE UNIVERSITY · PI Jorn Coers · 2024 to 2026
$1.6M
Regulation of Intestinal Inflammation by Irgm1I01BX002369 · VA · DURHAM VA MEDICAL CENTER · PI TAYLOR, GREGORY A · 2015 to 2018
–
BLRD VA I01 BX002369NIAID NIH HHS R01 AI057831NIAID NIH HHS R01 AI088100NIAID NIH HHS R37 AI103197NIAID NIH HHS UC6 AI058607NIDDK NIH HHS R01 DK106090
6 · The paper itself

Abstract

The immunity-related GTPases (IRGs) are a family of proteins that are induced by interferon (IFN)-γ and play pivotal roles in immune and inflammatory responses. IRGs ostensibly function as dynamin-like proteins that bind to intracellular membranes and promote remodeling and trafficking of those membranes. Prior studies have shown that loss of Irgm1 in mice leads to increased lethality to bacterial infections as well as enhanced inflammation to non-infectious stimuli; however, the mechanisms underlying these phenotypes are unclear. In the studies reported here, we found that uninfected Irgm1-deficient mice displayed high levels of serum cytokines typifying profound autoinflammation. Similar increases in cytokine production were also seen in cultured, IFN-γ-primed macrophages that lacked Irgm1. A series of metabolic studies indicated that the enhanced cytokine production was associated with marked metabolic changes in the Irgm1-deficient macrophages, including increased glycolysis and an accumulation of long chain acylcarnitines. Cells were exposed to the glycolytic inhibitor, 2-deoxyglucose, or fatty acid synthase inhibitors to perturb the metabolic alterations, which resulted in dampening of the excessive cytokine production. These results suggest that Irgm1 deficiency drives metabolic dysfunction in macrophages in a manner that is cell-autonomous and independent of infectious triggers. This may be a significant contributor to excessive inflammation seen in Irgm1-deficient mice in different contexts.

Indexed as

AnimalsAutophagyCells, CulturedCytokinesGene DeletionGlycolysisGTP-Binding ProteinsInflammationInterferon-gammaMacrophagesMiceCytokinesGTP-Binding ProteinsIfi1 protein, mouseInterferon-gammacytokine inductionfatty acid metabolismglycolysisimmunity-related GTPaseinterferon gammaIrgm1macrophagerespiration

Identifiers

PMID28154172
PMCPMC5377780
OpenAlexW2585384292

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.