Evidence map›Paper›PMID 31486847›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2019

TIPE2 ameliorates lipopolysaccharide-induced apoptosis and inflammation in acute lung injury.

Xiaojing Wu, Qian Kong, Liying Zhan, Zhen Qiu, Qin Huang, Xuemin Song

Open access · bronzeAbstract read
In one paragraph

Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

29 citing papers in PubMed, 73 citations in OpenAlex.

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  20. Regulation of inflammation and apoptosis by GPR43 via JNK/ELK1 in acute lung injury.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022
    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

6 authors at 3 institutions in 1 country.

Xiaojing WuDepartment of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China.
Qian KongDepartment of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China.
Liying ZhanDepartment of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China.
Zhen QiuDepartment of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China.
Qin HuangDepartment of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China.
Xuemin SongDepartment of Anesthesiology and Critical Care Medicine, Zhongnan Hospital of Wuhan University, Wuhan, Hubei Province, China. sxmcl1018@163.com.
Wuhan University · CNRenmin Hospital of Wuhan University · CNZhongnan Hospital of Wuhan University · CN

Funding

National Natural Science Foundation of China 81571941
6 · The paper itself

Abstract

objectiveTumour necrosis factor-α-induced protein 8-like 2 (TIPE2) has strong anti-inflammatory properties. However, it is unknown whether increased TIPE2 is protective against lipopolysaccharide (LPS)-induced ALI. In the current study, we aimed to investigate whether increased TIPE2 can exert protective effects in a mouse model of ALI induced by LPS.

methodsWe administered TIPE2 adeno-associated virus (AAV-TIPE2) intratracheally into the lungs of mice. Three weeks later, ALI was induced by intratracheal injection of LPS into BALB/c mice. Twenty-four hours later, lung bronchoalveolar lavage fluid (BALF) was acquired to analyse cells and protein, arterial blood was collected for arterial blood gas analysis and the determination of pro-inflammatory factor levels, and lung issues were collected for histologic examination, transmission electron microscopy (TEM), TUNEL staining, wet/dry (W/D) weight ratio analysis, myeloperoxidase (MPO) activity analysis and blot analysis of protein expression.

resultsWe found that TIPE2 overexpression markedly mitigated LPS-induced lung injury, which was evaluated by the deterioration of histopathology, histologic scores, the W/D weight ratio, and total protein expression in the BALF. Moreover, TIPE2 overexpression markedly attenuated lung inflammation, as evidenced by the downregulation of polymorphonuclear neutrophils (PMNs) in the BALF, lung MPO activity, and pro-inflammatory cytokine levels in the serum. Moreover, TIPE2 overexpression not only dramatically prevented LPS-induced pulmonary cell apoptosis in mice but also blocked LPS-activated JNK phosphorylation and NF-κB p65 nuclear translocation.

conclusionsOur study shows that the increased expression of AAV-mediated TIPE2 in the lungs of mice inhibits acute inflammation and apoptosis and suppresses the activation of NF-κB and JNK in a murine model of ALI.

Indexed as

Acute Lung InjuryAnimalsApoptosisBronchoalveolar Lavage FluidCytokinesDependovirusInflammationIntracellular Signaling Peptides and ProteinsJNK Mitogen-Activated Protein KinasesLeukocyte CountLipopolysaccharidesLungMaleMice, Inbred BALB CMicroscopy, Electron, TransmissionNF-kappa BCytokinesIntracellular Signaling Peptides and ProteinsJNK Mitogen-Activated Protein KinasesLipopolysaccharidesNF-kappa BTIPE2 protein, mouseAcute lung injuryApoptosisCytokinesInflammationJNKNF-κBTIPE2

Identifiers

PMID31486847
PMCPMC7096061
OpenAlexW2971916320

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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.