Evidence map›Paper›PMID 28144894›Full record

ArticleDigestive diseases and sciences2017

Tumor Necrosis Factor α-Dependent Neutrophil Priming Prevents Intestinal Ischemia/Reperfusion-Induced Bacterial Translocation.

Yen-Zhen Lu, Ching-Ying Huang, Yi-Cheng Huang, Tsung-Chun Lee, Wei-Ting Kuo, Yu-Chen Pai, Linda Chia-Hui Yu

Abstract read
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In one paragraph

Article in Digestive diseases and sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.8field-weighted citation impact, top 31% 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

9 citing papers in PubMed, 14 citations in OpenAlex.

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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 1 institution in 1 country.

Yen-Zhen LuGraduate Institute of Physiology, National Taiwan University College of Medicine, Suite 1020, #1 Jen-Ai Rd. Sec. I, Taipei 100, Taiwan, ROC.
Ching-Ying HuangGraduate Institute of Physiology, National Taiwan University College of Medicine, Suite 1020, #1 Jen-Ai Rd. Sec. I, Taipei 100, Taiwan, ROC.
Yi-Cheng HuangGraduate Institute of Physiology, National Taiwan University College of Medicine, Suite 1020, #1 Jen-Ai Rd. Sec. I, Taipei 100, Taiwan, ROC.
Tsung-Chun LeeGraduate Institute of Physiology, National Taiwan University College of Medicine, Suite 1020, #1 Jen-Ai Rd. Sec. I, Taipei 100, Taiwan, ROC.
Wei-Ting KuoGraduate Institute of Physiology, National Taiwan University College of Medicine, Suite 1020, #1 Jen-Ai Rd. Sec. I, Taipei 100, Taiwan, ROC.
Yu-Chen PaiGraduate Institute of Physiology, National Taiwan University College of Medicine, Suite 1020, #1 Jen-Ai Rd. Sec. I, Taipei 100, Taiwan, ROC.
Linda Chia-Hui YuGraduate Institute of Physiology, National Taiwan University College of Medicine, Suite 1020, #1 Jen-Ai Rd. Sec. I, Taipei 100, Taiwan, ROC. lchyu@ntu.edu.tw.ORCID 0000-0003-1461-3249
National Taiwan University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIntestinal ischemia/reperfusion (I/R) causes barrier impairment and bacterial influx. Protection against I/R injury in sterile organs by hypoxic preconditioning (HPC) had been attributed to erythropoietic and angiogenic responses. Our previous study showed attenuation of intestinal I/R injury by HPC for 21 days in a neutrophil-dependent manner.

aimTo investigate the underlying mechanisms of neutrophil priming by HPC, and explore whether adoptive transfer of primed neutrophils is sufficient to ameliorate intestinal I/R injury.

methodsRats raised in normoxia (NM) and HPC for 3 or 7 days were subjected to sham operation or superior mesenteric artery occlusion for I/R challenge. Neutrophils isolated from rats raised in NM or HPC for 21 days were intravenously injected into naïve controls prior to I/R.

resultsSimilar to the protective effect of HPC-21d, I/R-induced mucosal damage was attenuated by HPC-7d but not by HPC-3d. Naïve rats reconstituted with neutrophils of HPC-21d rats showed increase in intestinal phagocytic infiltration and myeloperoxidase activity, and barrier protection against I/R insult. Elevated free radical production, and higher bactericidal and phagocytic activity were observed in HPC neutrophils compared to NM controls. Moreover, increased serum levels of tumor necrosis factor α (TNFα) and cytokine-induced neutrophil chemoattractant-1 (CINC-1) were seen in HPC rats. Naïve neutrophils incubated with HPC serum or recombinant TNFα, but not CINC-1, exhibited heightened respiratory burst and bactericidal activity. Lastly, neutrophil priming effect was abolished by neutralization of TNFα in HPC serum.

conclusionsTNFα-primed neutrophils by HPC act as effectors cells for enhancing barrier integrity under gut ischemia.

Indexed as

Bacterial TranslocationIschemic PreconditioningAnimalsBlood Bactericidal ActivityCells, CulturedChemokine CXCL1Free RadicalsIntestinal MucosaIntestinesMaleNeutrophil ActivationNeutrophilsPhagocytosisRatsRats, WistarRecombinant ProteinsChemokine CXCL1Cxcl1 protein, ratFree RadicalsRecombinant ProteinsTumor Necrosis Factor-alphaBacterial influxEpithelial barrierIntermittent hypoxiaIntestinal ischemiaNeutrophil activityTumor necrosis factor

Identifiers

PMID28144894
OpenAlexW2585632318

What OpenQuestion holds

Textmetadata
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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.