Evidence map›Paper›PMID 27389701›Full record

ArticlePLoS pathogens2016

Annexin A2 Modulates ROS and Impacts Inflammatory Response via IL-17 Signaling in Polymicrobial Sepsis Mice.

Sisi He, Xuefeng Li, Rongpeng Li, Lizhu Fang, Lingyun Sun, Yongsheng Wang, Min Wu

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
3.1field-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

49 citing papers in PubMed, 104 citations in OpenAlex.

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  12. Annexin A2: A Double-Edged Sword in Pathogen Infection.Pathogens (Basel, Switzerland) · 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

7 authors at 3 institutions in 2 countries.

Sisi HeState Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, and Collaborative Innovation Center for Biotherapy, Chengdu, Sichuan, P. R. China.
Xuefeng LiState Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, and Collaborative Innovation Center for Biotherapy, Chengdu, Sichuan, P. R. China.
Rongpeng LiDepartment of Biomedical Sciences, University of North Dakota, Grand Forks, North Dakota, United States of America.
Lizhu FangDepartment of Biomedical Sciences, University of North Dakota, Grand Forks, North Dakota, United States of America.
Lingyun SunDepartment of Rheumatology and Immunology, The Affiliated Drum Tower Hospital, Nanjing University Medical School, Nanjing, Jiangsu, P. R. China.ORCID 0000-0002-5498-4709
Yongsheng WangState Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, and Collaborative Innovation Center for Biotherapy, Chengdu, Sichuan, P. R. China.
Min WuDepartment of Biomedical Sciences, University of North Dakota, Grand Forks, North Dakota, United States of America.
Sichuan University · CNUniversity of North Dakota · USNanjing Drum Tower Hospital · CN

Funding

Pilot Projects CoreP30GM103329 · NIGMS · UNIVERSITY OF NORTH DAKOTA · PI GEIGER, JONATHAN DAVID · 2012 to 2016
$5.1M
Lung innate immunity against bacterial infectionR01AI109317 · NIAID · UNIVERSITY OF NORTH DAKOTA · PI WU, MIN · 2014 to 2018
$1.7M
Lung epithelium collaborates with alveolar macrophages in host defenseR15AI101973 · NIAID · UNIVERSITY OF NORTH DAKOTA · PI WU, MIN · 2012 to 2012
$414k
Ceramide membrane microdomains regulate cytokine secretionR03AI097532 · NIAID · UNIVERSITY OF NORTH DAKOTA · PI SINGH, BRIJ B · 2012 to 2013
$138k
NIAID NIH HHS R01 AI109317NIAID NIH HHS R03 AI097532NIAID NIH HHS R15 AI101973NIGMS NIH HHS P30 GM103329
6 · The paper itself

Abstract

Sepsis is a progressive disease manifesting excessive inflammatory responses, severe tissue injury, organ dysfunction, and, ultimately, mortality. Since currently, there are limited therapeutic options for this disease, further understanding the molecular pathogenesis of sepsis may help develop effective treatments. Here we identify a novel role for Annexin A2 (AnxA2), a multi-compartmental protein, in inhibiting pro-inflammatory response by regulating reactive oxygen species (ROS) and IL-17 signaling during sepsis. In cecal ligation and puncture (CLP) sepsis models, anxa2-/- mice manifested increased pro-inflammatory cytokines and neutrophil infiltration, but decreased bacterial clearance and animal survival. In addition, AnxA2 deficiency led to intensified ROS and IL-17A. Using site directed mutagenesis, we uncovered that cysteine 9 of AnxA2 was the most important aa (site) for regulation of ROS levels. Furthermore, ROS appears to be responsible for elevated IL-17A levels and subsequently exaggerated inflammatory response. Depletion of IL-17 via CRISPR/Cas9 KO strategy down-regulated inflammation and conferred protection against sepsis in anxa2-/- mice. Our findings reveal a previously undemonstrated function for AnxA2 in inflammatory response in polymicrobial sepsis models via an AnxA2-ROS-IL-17 axis, providing insight into the regulation of pathophysiology of sepsis.

Indexed as

AnimalsAnnexin A2Disease Models, AnimalEnzyme-Linked Immunosorbent AssayFemaleFlow CytometryImmunoblottingInflammationInterleukin-17MiceMice, Inbred C57BLMice, KnockoutMutagenesis, Site-DirectedOligonucleotide Array Sequence AnalysisPolymerase Chain ReactionReactive Oxygen SpeciesAnnexin A2Interleukin-17Reactive Oxygen Species

Identifiers

PMID27389701
PMCPMC4936746
OpenAlexW2472819017

What OpenQuestion holds

Textmetadata
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.