Evidence map›Paper›PMID 26692926›Full record

ArticleAmerican journal of translational research2015

AAL exacerbates pro-inflammatory response in macrophages by regulating Mincle/Syk/Card9 signaling along with the Nlrp3 inflammasome assembly.

Zhijun Zhang, Long He, Shuang Hu, Yi Wang, Qiaohong Lai, Ping Yang, Qilin Yu, Shu Zhang, Fei Xiong, Sakine Simsekyilmaz and 8 more

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

8 citing papers in PubMed, 22 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

18 authors at 3 institutions in 1 country.

Zhijun ZhangThe Center for Biomedical Research, Institute of Infectious Disease, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology 1095 Jiefang Ave., Wuhan 430030, China.
Long HeThe Center for Biomedical Research, Institute of Infectious Disease, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology 1095 Jiefang Ave., Wuhan 430030, China.
Shuang HuThe Center for Biomedical Research, Institute of Infectious Disease, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology 1095 Jiefang Ave., Wuhan 430030, China.
Yi WangThe Center for Biomedical Research, Institute of Infectious Disease, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology 1095 Jiefang Ave., Wuhan 430030, China.
Qiaohong LaiThe Center for Biomedical Research, Institute of Infectious Disease, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology 1095 Jiefang Ave., Wuhan 430030, China.
Ping YangThe Center for Biomedical Research, Institute of Infectious Disease, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology 1095 Jiefang Ave., Wuhan 430030, China.
Qilin YuThe Center for Biomedical Research, Institute of Infectious Disease, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology 1095 Jiefang Ave., Wuhan 430030, China.
Shu ZhangThe Center for Biomedical Research, Institute of Infectious Disease, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology 1095 Jiefang Ave., Wuhan 430030, China.
Fei XiongThe Center for Biomedical Research, Institute of Infectious Disease, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology 1095 Jiefang Ave., Wuhan 430030, China.
Sakine SimsekyilmazThe Center for Biomedical Research, Institute of Infectious Disease, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology 1095 Jiefang Ave., Wuhan 430030, China.
Qin NingDepartment of Infectious Disease, Institute of Infectious Disease, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology 1095 Jiefang Ave., Wuhan 430030, China.
Jinxiu LiDepartment of Emergency Medicine, Institute of Emergency Medicine and Rare Diseases, The Second Xiangya Hospital, Central South University Changsha, China.
Dongshan ZhangDepartment of Emergency Medicine, Institute of Emergency Medicine and Rare Diseases, The Second Xiangya Hospital, Central South University Changsha, China.
Hongliang ZhangDepartment of Emergency Medicine, Institute of Emergency Medicine and Rare Diseases, The Second Xiangya Hospital, Central South University Changsha, China.
Xudong XiangDepartment of Emergency Medicine, Institute of Emergency Medicine and Rare Diseases, The Second Xiangya Hospital, Central South University Changsha, China.
Zhiguang ZhouDiabetes Center, Key Laboratory of Diabetes Immunology, The Second Xiangya Hospital, Central South University Changsha, China.
Hui SunCollege of Life Sciences, Wuhan University Wuhan, China.
Cong-Yi WangThe Center for Biomedical Research, Institute of Infectious Disease, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology 1095 Jiefang Ave., Wuhan 430030, China.
Tongji Hospital · CNCentral South University · CNWuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previously, we demonstrated that Agrocybe aegerita lectin (AAL), a galectin isolated from edible mushroom Agrocybe aegerita, exerts potent anti-tumor activity, while the mechanisms by which AAL suppresses tumor growth are yet to be elucidated. Here, we conducted studies with focus for its impact on the cecal ligation and puncture (CLP)-induced innate immune response. Administration of AAL significantly exacerbated the severity of CLP-induced septic shock as manifested the increased lethality. AAL promoted inflammatory cytokine production by preferentially regulating macrophage activation and recruitment. Mechanistic studies revealed that AAL likely targets macrophages through receptor Mincle to activate Syk/Card9 signaling, which then couples to the Nlrp3 inflammasome assembly. It was further noted that AAL markedly promotes H3K4 di- and trimethylation, by which it enhances Hmgb1 expression. Specifically, AAL induced macrophages secretion of copious amount of Hmgb1 as manifested the Hmgb1 cytoplasmic translocation along with the detection of extracellular Hmgb1. AAL also stimulated a significant increase for nuclear Hmgb1, which then formed a complex with RelA, and thereby enhancing NF-κB transcriptional activity. Together, our data suggest that AAL may possess important pharmaceutical properties in the regulation of innate immune response.

Indexed as

AALCLPHmgb1innate immunitymethylationmincleNF-κBNlrp3 inflammasomeseptic shock

Identifiers

PMID26692926
PMCPMC4656759
OpenAlexW2196765803

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.