Evidence map›Paper›PMID 26936883›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2016

Human SR-BI and SR-BII Potentiate Lipopolysaccharide-Induced Inflammation and Acute Liver and Kidney Injury in Mice.

Irina N Baranova, Ana C P Souza, Alexander V Bocharov, Tatyana G Vishnyakova, Xuzhen Hu, Boris L Vaisman, Marcelo J Amar, Zhigang Chen, Yana Kost, Alan T Remaley and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2016. 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
3.7field-weighted citation impact, top 7% 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, 70 citations in OpenAlex.

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  18. Scavenger Receptor BI Attenuates IL-17A-Dependent Neutrophilic Inflammation in Asthma.American journal of respiratory cell and molecular biology · 2021
    Article
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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

14 authors at 2 institutions in 1 country.

Irina N BaranovaDepartment of Laboratory Medicine, Clinical Center, National Institutes of Health, Bethesda, MD 20892;ORCID http://orcid.org/0000-0003-4250-1340
Ana C P SouzaRenal Diagnostics and Therapeutics Unit, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892;
Alexander V BocharovDepartment of Laboratory Medicine, Clinical Center, National Institutes of Health, Bethesda, MD 20892; eggermant@niddk.nih.gov abocharov@cc.nih.gov.ORCID http://orcid.org/0000-0002-3482-2980
Tatyana G VishnyakovaDepartment of Laboratory Medicine, Clinical Center, National Institutes of Health, Bethesda, MD 20892;
Xuzhen HuRenal Diagnostics and Therapeutics Unit, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892;
Boris L VaismanNational Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892; and.ORCID http://orcid.org/0000-0003-0495-2220
Marcelo J AmarNational Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892; and.ORCID http://orcid.org/0000-0002-9097-2422
Zhigang ChenDepartment of Laboratory Medicine, Clinical Center, National Institutes of Health, Bethesda, MD 20892;
Yana KostDepartment of Laboratory Medicine, Clinical Center, National Institutes of Health, Bethesda, MD 20892;
Alan T RemaleyNational Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892; and.
Amy P PattersonDepartment of Laboratory Medicine, Clinical Center, National Institutes of Health, Bethesda, MD 20892; National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892; and.
Peter S T YuenRenal Diagnostics and Therapeutics Unit, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892;ORCID http://orcid.org/0000-0001-9557-3909
Robert A StarRenal Diagnostics and Therapeutics Unit, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892;ORCID http://orcid.org/0000-0003-0940-3079
Thomas L EggermanDepartment of Laboratory Medicine, Clinical Center, National Institutes of Health, Bethesda, MD 20892; Division of Diabetes, Endocrinology, and Metabolic Diseases, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892.
National Institutes of Health · USNational Institutes of Health Clinical Center · US

Funding

NHLBI Animal Program DivisionZIGHL006020 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI CLARK, TANNIA · 2009 to 2025
$47.3M
Inhibition Of Renal InjuryZIADK043403 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI STAR, ROBERT A · 2009 to 2025
$15.5M
Intramural NIH HHS Z99 DK999999
6 · The paper itself

Abstract

The class B scavenger receptors BI (SR-BI) and BII (SR-BII) are high-density lipoprotein receptors that recognize various pathogens, including bacteria and their products. It has been reported that SR-BI/II null mice are more sensitive than normal mice to endotoxin-induced inflammation and sepsis. Because the SR-BI/II knockout model demonstrates multiple immune and metabolic disorders, we investigated the role of each receptor in the LPS-induced inflammatory response and tissue damage using transgenic mice with pLiv-11-directed expression of human SR-BI (hSR-BI) or human SR-BII (hSR-BII). At 6 h after i.p. LPS injection, transgenic hSR-BI and hSR-BII mice demonstrated markedly higher serum levels of proinflammatory cytokines and 2- to 3-fold increased expression levels of inflammatory mediators in the liver and kidney, compared with wild-type (WT) mice. LPS-stimulated inducible NO synthase expression was 3- to 6-fold higher in the liver and kidney of both transgenic strains, although serum NO levels were similar in all mice. Despite the lower high-density lipoprotein plasma levels, both transgenic strains responded to LPS by a 5-fold increase of plasma corticosterone levels, which were only moderately lower than in WT animals. LPS treatment resulted in MAPK activation in tissues of all mice; however, the strongest response was detected for hepatic extracellular signal-regulated protein kinase 1 and 2 and kidney JNK of both transgenic mice. Histological examination of hepatic and renal tissue from LPS-challenged mice revealed more injury in hSR-BII, but not hSR-BI, transgenic mice versus WT controls. Our findings demonstrate that hSR-BII, and to a lesser extent hSR-BI, significantly increase LPS-induced inflammation and contribute to LPS-induced tissue injury in the liver and kidney, two major organs susceptible to LPS toxicity.

Indexed as

Acute Kidney InjuryAnimalsCD36 AntigensCell LineCytokinesDisease Models, AnimalGene ExpressionHumansInflammationInflammation MediatorsLipopolysaccharidesLiver DiseasesLysosomal Membrane ProteinsMacrophagesMiceMice, TransgenicCD36 AntigensCytokinesInflammation MediatorsLipopolysaccharidesLysosomal Membrane ProteinsMitogen-Activated Protein KinasesNitric Oxide SynthaseReceptors, ScavengerRNA, MessengerSCARB2 protein, human

Identifiers

PMID26936883
PMCPMC4856165
OpenAlexW2289669280

What OpenQuestion holds

Textmetadata
LicenceTDM
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.