Evidence map›Paper›PMID 27625297›Full record

ArticleScientific reports2016

Splenic CD11c(low)CD45RB(high) dendritic cells derived from endotoxin-tolerant mice attenuate experimental acute liver failure.

Sai-Nan Zhang, Nai-Bin Yang, Shun-Lan Ni, Jin-Zhong Dong, Chun-Wei Shi, Shan-Shan Li, Sheng-Guo Zhang, Xin-Yue Tang, Ming-Qin Lu

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.6field-weighted citation impact, top 30% 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

4 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Postpartum uterine infection & ovarian dysfunction.The Indian journal of medical research · 2018
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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

9 authors at 4 institutions in 1 country.

Sai-Nan ZhangDepartment of Infection Diseases, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou Key Laboratory of Hepatology, Hepatology Institute of Wenzhou Medical University, Wenzhou 325000, Zhejiang, P. R. China.
Nai-Bin YangDepartment of Infection Diseases, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou Key Laboratory of Hepatology, Hepatology Institute of Wenzhou Medical University, Wenzhou 325000, Zhejiang, P. R. China.
Shun-Lan NiDepartment of Infection Diseases, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou Key Laboratory of Hepatology, Hepatology Institute of Wenzhou Medical University, Wenzhou 325000, Zhejiang, P. R. China.
Jin-Zhong DongDepartment of Intensive Care Unit, The First Hospital of Ningbo, Ningbo 315010, Zhejiang, P. R. China.
Chun-Wei ShiDepartment of Infection Diseases, The First Hospital of Xiaoshan, Hangzhou 311200, Zhejiang, P. R. China.
Shan-Shan LiDepartment of Infection Diseases, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou Key Laboratory of Hepatology, Hepatology Institute of Wenzhou Medical University, Wenzhou 325000, Zhejiang, P. R. China.
Sheng-Guo ZhangDepartment of Infection Diseases, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou Key Laboratory of Hepatology, Hepatology Institute of Wenzhou Medical University, Wenzhou 325000, Zhejiang, P. R. China.
Xin-Yue TangDepartment of Infection Diseases, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou Key Laboratory of Hepatology, Hepatology Institute of Wenzhou Medical University, Wenzhou 325000, Zhejiang, P. R. China.
Ming-Qin LuDepartment of Infection Diseases, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou Key Laboratory of Hepatology, Hepatology Institute of Wenzhou Medical University, Wenzhou 325000, Zhejiang, P. R. China.
Wenzhou Medical University · CNFirst Affiliated Hospital of Wenzhou Medical University · CNNingbo First Hospital · CNThe First People's Hospital of Xiaoshan District, Hangzhou · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endotoxin tolerance (ET) is suggested to attenuate the severity of acute liver failure (ALF) in mice, possibly through both innate and adaptive immunity. However, the involvement of regulatory dendritic cells (DCregs) in ET has not been fully elucidated. In this study, their effect on ALF in mice was investigated. Splenic DCregs from ET-exposed mice (ET-DCregs) showed lower expression levels of CD40, CD80, and MHC-II markers and stronger inhibition of allogenic T cells and regulation of IL-10 and IL-12 secretion than splenic DCregs from normal mice (nDCregs). Moreover, the mRNA and protein levels of TNF-α and P65 in splenic ET-DCregs were significantly lower than those in the splenic nDCregs. The survival rate was significantly increased and liver injury was mitigated in mice with ALF treated with splenic ET-DCregs. In addition, A20 expression was decreased in the liver of ALF mice, but elevated after infusion of splenic nDCregs and ET-DCregs, and a much higher elevation was observed after infusing the latter cells. The functionality of splenic DCregs was altered after ET exposure, contributing to protection of the livers against D-GalN/LPS-induced ALF.

Indexed as

Disease ResistanceAnimalsCD11c AntigenCytokinesDendritic CellsLeukocyte Common AntigensLipopolysaccharidesLiver Failure, AcuteMaleMiceMice, Inbred BALB CSpleenCD11c AntigenCytokinesLeukocyte Common AntigensLipopolysaccharidesPtprc protein, mouse

Identifiers

PMID27625297
PMCPMC5021931
OpenAlexW2520331856

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Registered trials

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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.