Evidence map›Paper›PMID 26810228›Full record

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

Subclinical-Dose Endotoxin Sustains Low-Grade Inflammation and Exacerbates Steatohepatitis in High-Fat Diet-Fed Mice.

Honghui Guo, Na Diao, Ruoxi Yuan, Keqiang Chen, Shuo Geng, Mingsong Li, Liwu Li

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 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.1field-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

23 citing papers in PubMed, 35 citations in OpenAlex.

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  18. Next generation probiotics in disease amelioration.Journal of food and drug analysis · 2019
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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

7 authors at 3 institutions in 2 countries.

Honghui Guo *Laboratory of Inflammation Biology, Department of Biological Sciences, Virginia Tech, Blacksburg, Virginia 24061-0910, USA.
Na Diao *Laboratory of Inflammation Biology, Department of Biological Sciences, Virginia Tech, Blacksburg, Virginia 24061-0910, USA.
Ruoxi YuanLaboratory of Inflammation Biology, Department of Biological Sciences, Virginia Tech, Blacksburg, Virginia 24061-0910, USA.
Keqiang ChenLaboratory of Inflammation Biology, Department of Biological Sciences, Virginia Tech, Blacksburg, Virginia 24061-0910, USA.
Shuo GengLaboratory of Inflammation Biology, Department of Biological Sciences, Virginia Tech, Blacksburg, Virginia 24061-0910, USA.
Mingsong LiDepartment of Gastroenterology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Liwu LiLaboratory of Inflammation Biology, Department of Biological Sciences, Virginia Tech, Blacksburg, Virginia 24061-0910, USA.
Shaoguan University · CNVirginia Tech · USNanfang Hospital · CN

Funding

Modulation of innate immune cellular homeostasis and inflammation resolutionR01HL115835 · NHLBI · VIRGINIA POLYTECHNIC INST AND ST UNIV · PI LI, LIWU · 2012 to 2021
$3.6M
NHLBI NIH HHS R01 HL115835NHLBI NIH HHS R01 HL135835
6 · The paper itself

Abstract

Subclinical circulating bacterial endotoxin LPS has been implicated as an important cofactor in the development and progression of nonalcoholic steatohepatitis, but the underlying mechanisms remain unclear. In this study, we demonstrated that 4-wk injection with superlow-dose LPS significantly promoted neutrophil infiltration and accelerated nonalcoholic steatohepatitis progression, including exacerbated macrovesicular steatosis, inflammation, and hepatocyte ballooning in high-fat diet-fed apolipoprotein E knockout mice. This effect could sustain for a month after stoppage of LPS injection. LPS also significantly increased numbers of apoptotic nuclei in hepatocytes and expressions of proapoptotic regulators. Moreover, LPS sustained the low-grade activation of p38 MAPK and inhibited the expression of the upstream MAPK phosphatase 7. By applying selective inhibitors, we demonstrated that the activation of p38 MAPKs is required for neutrophil migration induced by superlow-dose LPS in vitro. Together, these data suggest that superlow-dose LPS may sustain the low-grade activation of p38 MAPKs and neutrophil infiltration, leading to the exacerbation of steatohepatitis.

Indexed as

AnimalsApolipoproteins EApoptosisChemotaxis, LeukocyteDiet, High-FatDisease Models, AnimalDisease ProgressionDual-Specificity PhosphatasesEndotoxinsLipid MetabolismLipidsLipopolysaccharidesLiverMacrophagesMaleMAP Kinase Signaling SystemApolipoproteins EDual-Specificity PhosphatasesDusp16 protein, mouseEndotoxinsLipidsLipopolysaccharidesMitogen-Activated Protein Kinase Phosphatasesp38 Mitogen-Activated Protein Kinases

Identifiers

PMID26810228
PMCPMC4761480
OpenAlexW2257366303

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.