Evidence map›Paper›PMID 23527230›Full record

ArticlePloS one2013

Galectin-3 functions as an alarmin: pathogenic role for sepsis development in murine respiratory tularemia.

Bibhuti B Mishra, Qun Li, Anthony L Steichen, Brandilyn J Binstock, Dennis W Metzger, Judy M Teale, Jyotika Sharma

Open access · goldAbstract readComparative Study
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

44 citing papers in PubMed, 67 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. The Role of Galectin-3 in Liver Inflammation and Fibrosis.Journal of inflammation research · 2026
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Galectin-3 Inhibition in COVID-19.American journal of respiratory and critical care medicine · 2023
    Article
  12. Article
  13. Article
  14. Observational
  15. Gal3 Plays a Deleterious Role in a Mouse Model of Endotoxemia.International journal of molecular sciences · 2022
    Article
  16. Article
  17. Observational
  18. Article
  19. Transcriptomic responses from improved murine sepsis models can better mimic human surgical sepsis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    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

7 authors at 3 institutions in 1 country.

Bibhuti B MishraDepartment of Microbiology and Immunology, University of North Dakota School of Medicine and Health Sciences, Grand Forks, North Dakota, United States of America.
Qun Li
Anthony L Steichen
Brandilyn J Binstock
Dennis W Metzger
Judy M Teale
Jyotika Sharma
University of North Dakota · USTexas Center for Infectious Disease · USAlbany Medical Center Hospital · US

Funding

TLR2/NLR Signal Regulation of Protective Immunity to F. TularensisP01AI056320 · NIAID · ALBANY MEDICAL COLLEGE · PI METZGER, DENNIS W · 2003 to 2016
$22.9M
Mechanism of sepsis development in pulmonary bacterial infectionR21AI101644 · NIAID · UNIVERSITY OF NORTH DAKOTA · PI SHARMA, JYOTIKA · 2012 to 2013
$387k
NIAID NIH HHS 1R21AI101644-01NIAID NIH HHS P01 AI056320NIAID NIH HHS R21 AI101644PHS HHS 1P01A10157986
6 · The paper itself

Abstract

Sepsis is a complex immune disorder with a mortality rate of 20-50% and currently has no therapeutic interventions. It is thus critical to identify and characterize molecules/factors responsible for its development. We have recently shown that pulmonary infection with Francisella results in sepsis development. As extensive cell death is a prominent feature of sepsis, we hypothesized that host endogenous molecules called alarmins released from dead or dying host cells cause a hyperinflammatory response culminating in sepsis development. In the current study we investigated the role of galectin-3, a mammalian β-galactoside binding lectin, as an alarmin in sepsis development during F. novicida infection. We observed an upregulated expression and extracellular release of galectin-3 in the lungs of mice undergoing lethal pulmonary infection with virulent strain of F. novicida but not in those infected with a non-lethal, attenuated strain of the bacteria. In comparison with their wild-type C57Bl/6 counterparts, F. novicida infected galectin-3 deficient (galectin-3(-/-)) mice demonstrated significantly reduced leukocyte infiltration, particularly neutrophils in their lungs. They also exhibited a marked decrease in inflammatory cytokines, vascular injury markers, and neutrophil-associated inflammatory mediators. Concomitantly, in-vitro pre-treatment of primary neutrophils and macrophages with recombinant galectin-3 augmented F. novicida-induced activation of these cells. Correlating with the reduced inflammatory response, F. novicida infected galectin-3(-/-) mice exhibited improved lung architecture with reduced cell death and improved survival over wild-type mice, despite similar bacterial burden. Collectively, these findings suggest that galectin-3 functions as an alarmin by augmenting the inflammatory response in sepsis development during pulmonary F. novicida infection.

Indexed as

AnimalsAntibodies, MonoclonalCytokinesDNA PrimersFluorescent Antibody TechniqueGalectin 3Immunologic FactorsIn Situ Nick-End LabelingKaplan-Meier EstimateLungMiceMice, Inbred C57BLMice, KnockoutReal-Time Polymerase Chain ReactionRespiratory Tract InfectionsSepsisAntibodies, MonoclonalCytokinesDNA PrimersGalectin 3Immunologic Factors

Identifiers

PMID23527230
PMCPMC3603908
OpenAlexW1969644265

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.