Evidence map›Paper›PMID 24453428›Full record

ArticleMediators of inflammation2013

Alcohol-induced liver injury is modulated by Nlrp3 and Nlrc4 inflammasomes in mice.

David A DeSantis, Chih-Wei Ko, Yang Liu, Xiuli Liu, Amy G Hise, Gabriel Nunez, Colleen M Croniger

Open access · goldAbstract read
In one paragraph

Article in Mediators of inflammation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.8field-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

33 citing papers in PubMed, 64 citations in OpenAlex.

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  15. Aging · 2021
    Article
  16. Review
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  18. Article
  19. NLRP3 Inflammasome and IL-33: Novel Players in Sterile Liver Inflammation.International journal of molecular sciences · 2018
    Review
  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

7 authors at 4 institutions in 1 country.

David A DeSantisDepartments of Nutrition, Case Western Reserve University School of Medicine, 10900 Euclid Avenue, Cleveland, OH 44106, USA.
Chih-Wei KoDepartments of Nutrition, Case Western Reserve University School of Medicine, 10900 Euclid Avenue, Cleveland, OH 44106, USA.
Yang LiuDepartments of Nutrition, Case Western Reserve University School of Medicine, 10900 Euclid Avenue, Cleveland, OH 44106, USA.
Xiuli LiuDepartment of Anatomic Pathology, Cleveland Clinic, Cleveland, OH 4406, USA.
Amy G HiseDepartment of Pathology, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA ; Department of Medicine, Louis Stokes Cleveland Department of Veterans' Affairs Medical Center, Cleveland, OH 44106, USA ; Center for Global Health and Diseases, Case Western Reserve University, Cleveland, OH 44106, USA.
Gabriel NunezDepartment of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109, USA.
Colleen M CronigerDepartments of Nutrition, Case Western Reserve University School of Medicine, 10900 Euclid Avenue, Cleveland, OH 44106, USA.
University School · USCleveland Clinic · USLouis Stokes Cleveland VA Medical Center · USUniversity of Michigan · US

Funding

TRAINING IN METABOLISMT32DK007319 · NIDDK · CASE WESTERN RESERVE UNIVERSITY · PI BRUNENGRABER, HENRI · 1986 to 2013
$5.0M
Pilot ProjectP20AA017837 · NIAAA · CLEVELAND CLINIC LERNER COM-CWRU · PI NAGY, LAURA E. · 2009 to 2013
$2.2M
NIAAA NIH HHS P20 AA017837NIDDK NIH HHS T32 DK007319NIDDK NIH HHS T32-DK007319
6 · The paper itself

Abstract

Alcoholic liver disease (ALD) is characterized by increased hepatic lipid accumulation (steatosis) and inflammation with increased expression of proinflammatory cytokines. Two of these cytokines, interleukin-1 β (IL-1 β ) and IL-18, require activation of caspase-1 via members of the NOD-like receptor (NLR) family. These NLRs form an inflammasome that is activated by pathogens and signals released through local tissue injury or death. NLR family pyrin domain containing 3 (Nlrp3) and NLR family CARD domain containing protein 4 (Nlrc4) have been studied minimally for their role in the development of ALD. Using mice with gene targeted deletions for Nlrp3 (Nlrp3(-/-)) and Nlrc4 (Nlrc4(-/-)), we analyzed the response to chronic alcohol consumption. We found that Nlrp3(-/-) mice have more severe liver injury with higher plasma alanine aminotransferase (ALT) levels, increased activation of IL-18, and reduced activation of IL-1B. In contrast, the Nlrc4(-/-) mice had similar alcohol-induced liver injury compared to C57BL/6J (B6) mice but had greatly reduced activation of IL-1 β . This suggests that Nlrp3 and Nlrc4 inflammasomes activate IL-1 β and IL-18 via caspase-1 in a differential manner. We conclude that the Nlrp3 inflammasome is protective during alcohol-induced liver injury.

Indexed as

AnimalsApoptosis Regulatory ProteinsCalcium-Binding ProteinsCarrier ProteinsChemokine CCL2Choline DeficiencyInflammasomesInterleukin-18Interleukin-1betaLiver Diseases, AlcoholicMethionineMiceMice, Inbred C57BLNLR Family, Pyrin Domain-Containing 3 ProteinSTAT3 Transcription FactorTumor Necrosis Factor-alphaApoptosis Regulatory ProteinsCalcium-Binding ProteinsCarrier ProteinsCcl2 protein, mouseChemokine CCL2InflammasomesInterleukin-18Interleukin-1betaIpaf protein, mouseMethionineNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseStat3 protein, mouseSTAT3 Transcription FactorTumor Necrosis Factor-alpha

Identifiers

PMID24453428
PMCPMC3876912
OpenAlexW2117497424

What OpenQuestion holds

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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.