Evidence map›Paper›PMID 34507947›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2021

Macrophagic Extracellular Vesicle CXCL2 Recruits and Activates the Neutrophil CXCR2/PKC/NOX4 Axis in Sepsis.

Guozhen Wang, Weichang Huang, Shuanghu Wang, Jun Wang, Wanfu Cui, Wenyong Zhang, Anni Lou, Shiyu Geng, Xu Li

Open access · greenAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

35 citing papers in PubMed, 58 citations in OpenAlex.

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  19. Neutrophils-biology and diversity.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2024
    Review
  20. 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

9 authors at 2 institutions in 1 country.

Guozhen WangDepartment of Emergency Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, China; mylx99@smu.edu.cn.
Weichang HuangDepartment of Emergency Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Shuanghu WangThe Laboratory of Clinical Pharmacy, The People's Hospital of Lishui, Lishui, Zhejiang, China; and.ORCID 0000-0002-0057-267X
Jun WangState Key Laboratory of Organ Failure Research, Guangdong Provincial Key Laboratory of Viral Hepatitis Research, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Wanfu CuiDepartment of Emergency Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Wenyong ZhangDepartment of Emergency Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Anni LouDepartment of Emergency Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, China.ORCID 0000-0001-8223-9178
Shiyu GengDepartment of Emergency Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Xu LiDepartment of Emergency Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, China; mylx99@smu.edu.cn.
Nanfang Hospital · CNLishui City People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sepsis is a life-threatening organ dysfunction caused by a dysfunctional host response to infection. Neutrophils play a protective role by releasing antibacterial proteins or by phagocytizing bacteria. However, excess neutrophils can induce tissue damage. Recently, a novel intercellular communication pathway involving extracellular vesicles (EVs) has garnered considerable attention. However, whether EVs secreted by macrophages mediate neutrophil recruitment to infected sites has yet to be studied. In this study, we assessed the chemotactic effect of EVs isolated from mouse Raw264.7 macrophages on mouse neutrophils and found that CXCL2 was highly expressed in these EVs. By regulating CXCL2 in Raw264.7 macrophages, we found that CXCL2 on macrophage EVs recruited neutrophils in vitro and in vivo. The CXCL2 EVs activated the CXCR2/PKC/NOX4 pathway and induced tissue damage. This study provides information regarding the mechanisms underlying neutrophil recruitment to tissues and proposes innovative strategies and targets for the treatment of sepsis.

Indexed as

AnimalsCecumChemokine CXCL2Disease Models, AnimalExtracellular VesiclesImmune System DiseasesLeukocyte DisordersMacrophagesMiceMice, Inbred C57BLNADPH Oxidase 4Neutrophil ActivationNeutrophilsProtein Kinase CSepsisSignal TransductionChemokine CXCL2NADPH Oxidase 4Protein Kinase C

Identifiers

PMID34507947
PMCPMC8490939
OpenAlexW3197236462

What OpenQuestion holds

Textmetadata
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.