Evidence map›Paper›PMID 33868293›Full record

ArticleFrontiers in immunology2021

MicroLet-7b Regulates Neutrophil Function and Dampens Neutrophilic Inflammation by Suppressing the Canonical TLR4/NF-κB Pathway.

Binzhen Chen, Jia Han, Shaoheng Chen, Rufeng Xie, Jie Yang, Tongming Zhou, Qi Zhang, Rong Xia

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

30 citing papers in PubMed, 32 citations in OpenAlex.

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  19. A synbiotic mixture ofFrontiers in nutrition · 2024
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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

8 authors at 3 institutions in 1 country.

Binzhen ChenDepartment of Blood Transfusion, Huashan Hospital, Fudan University, Shanghai, China.
Jia HanDepartment of Blood Transfusion, Huashan Hospital, Fudan University, Shanghai, China.
Shaoheng ChenDepartment of Blood Transfusion, Huashan Hospital, Fudan University, Shanghai, China.
Rufeng XieBlood Engineering Laboratory, Shanghai Blood Center, Shanghai, China.
Jie YangBlood Engineering Laboratory, Shanghai Blood Center, Shanghai, China.
Tongming ZhouShanghai Key Laboratory of Data Science, School of Computer Science, Fudan University, Shanghai, China.
Qi ZhangDepartment of Blood Transfusion, Huashan Hospital, Fudan University, Shanghai, China.
Rong XiaDepartment of Blood Transfusion, Huashan Hospital, Fudan University, Shanghai, China.
Fudan University · CNHuashan Hospital · CNShanghai Blood Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sepsis is a heterogeneous syndrome caused by a dysregulated host response during the process of infection. Neutrophils are involved in the development of sepsis due to their essential role in host defense. COVID-19 is a viral sepsis. Disfunction of neutrophils in sepsis has been described in previous studies, however, little is known about the role of microRNA-let-7b (miR-let-7b), toll-like receptor 4 (TLR4), and nuclear factor kappa B (NF-κB) activity in neutrophils and how they participate in the development of sepsis. In this study, we investigated the regulatory pathway of miR-let-7b/TLR4/NF-κB in neutrophils. We also explored the downstream cytokines released by neutrophils following miR-let-7b treatment and its therapeutic effects in cecal ligation and puncture (CLP)-induced septic mice. Six-to-eight-week-old male C57BL/6 mice underwent CLP following treatment with miR-let-7b agomir. Survival (n=10), changes in liver and lungs histopathology (n=4), circulating neutrophil counts (n=4), the liver-body weight ratio (n=4-7), and the lung wet-to-dry ratio (n=5-6) were recorded. We found that overexpression of miR-let-7b could significantly down-regulate the expression of human-derived neutrophilic TLR4 at a post-transcriptional level, a decreased level of proinflammatory factors including interleukin-6 (IL-6), IL-8, tumor necrosis factor α (TNF-α), and an upregulation of anti-inflammatory factor IL-10

Indexed as

COVID-19HumansInflammationMicroRNAsNeutrophilsNF-kappa BSARS-CoV-2Signal TransductionToll-Like Receptor 4MicroRNAsmirnlet7 microRNA, humanNF-kappa BTLR4 protein, humanToll-Like Receptor 4COVID-19inflammationMicroLet-7bneutrophilsepsisTLR4/NF-κB

Identifiers

PMID33868293
PMCPMC8044834
OpenAlexW3147575837

What OpenQuestion holds

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LicenceCC BY
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.