Evidence map›Paper›PMID 31514375›Full record

ArticleCells2019

Lipocalin-2 (Lcn-2) Attenuates Polymicrobial Sepsis with LPS Preconditioning (LPS Tolerance) in FcGRIIb Deficient Lupus Mice.

Thunnicha Ondee, Joseph Gillen, Peerapat Visitchanakun, Poorichaya Somparn, Jiraphorn Issara-Amphorn, Cong Dang Phi, Wiwat Chancharoenthana, Devikala Gurusamy, Aleksandra Nita-Lazar, Asada Leelahavanichkul

Open access · goldAbstract read
In one paragraph

Article in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

30 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
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  3. Less Severe Lipopolysaccharide-Induced Inflammation in ConditionalInternational journal of molecular sciences · 2023
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  6. The Regulatory Roles ofInternational journal of molecular sciences · 2023
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  8. Frontiers in immunology · 2023
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  9. Review
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  13. Review
  14. Article
  15. Abnormal Blood Bacteriome, Gut Dysbiosis, and Progression to Severe Dengue Disease.Frontiers in cellular and infection microbiology · 2022
    Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article
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 at 2 institutions in 2 countries.

Thunnicha OndeeDepartment of Preventive and Social Medicine, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand.
Joseph GillenFunctional Cellular Networks Section, Laboratory of Immune System Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892-1892, USA.
Peerapat VisitchanakunDepartment of Microbiology, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand.
Poorichaya SomparnCenter of Excellence in Systems Biology, Research affairs, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand.ORCID 0000-0002-7422-1135
Jiraphorn Issara-AmphornDepartment of Microbiology, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand.
Cong Dang PhiDepartment of Microbiology, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand.
Wiwat ChancharoenthanaDepartment of Microbiology, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand.
Devikala GurusamySurgery Branch, National Cancer Institute, National Institutes of Health (NIH), Bethesda, MD 20892, USA.ORCID 0000-0002-1727-8653
Aleksandra Nita-LazarFunctional Cellular Networks Section, Laboratory of Immune System Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892-1892, USA.ORCID 0000-0002-8523-605X
Asada LeelahavanichkulDepartment of Preventive and Social Medicine, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand. a_leelahavanit@yahoo.com.ORCID 0000-0002-5566-6403
Chulalongkorn University · THNational Institutes of Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In patients with active lupus, spontaneous endotoxemia and possibly tolerance to lipopolysaccharide (LPS) is a potentially adverse complication. Similarly, previous reports have demonstrated that FcGRIIb deficient mice (FcGRIIb-/-; a lupus mouse model) are susceptible to LPS tolerance-induced decreased cytokine responses that inadequate for the organismal control. Thus, understanding the relationship between FcGRIIb and LPS tolerance could improve the therapeutic strategy for lupus. LPS tolerance can be induced through sequential LPS stimulations in either cells or a model organism. In RAW264.7 (a mouse macrophage cell-line), sequential LPS stimulation induced the secretion of Lipocalin-2 (Lcn-2) despite reduced cytokine secretion and severe energy depletion, as measured by the extracellular flux analysis, typical of LPS tolerance. In contrast, treatment with recombinant Lcn-2 (rLcn-2) attenuated LPS tolerance, as shown by an increase in secreted cytokines and altered macrophage polarization toward M1 (increased

Indexed as

Lipocalin-2AnimalsCytokinesDisease Models, AnimalEndotoxemiaImmune ToleranceLipopolysaccharidesLupus Erythematosus, SystemicMacrophagesMiceMice, Inbred C57BLRAW 264.7 CellsReceptors, IgGRecombinant ProteinsCytokinesFcgr2b protein, mouseLcn2 protein, mouseLipocalin-2LipopolysaccharidesReceptors, IgGRecombinant ProteinsFc gamma receptor IIb deficient macrophagesLipocalin 2lupusneutrophil gelatinase-associated lipocalin (NGAL)

Identifiers

PMID31514375
PMCPMC6769833
OpenAlexW2972721108

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.