Evidence map›Paper›PMID 35799057›Full record

ArticleCellular & molecular immunology2022

Dextran sodium sulfate potentiates NLRP3 inflammasome activation by modulating the KCa3.1 potassium channel in a mouse model of colitis.

Bo Zeng, Yuanting Huang, Siyuan Chen, Rong Xu, Lihui Xu, Jiahao Qiu, Fuli Shi, Siying Liu, Qingbing Zha, Dongyun Ouyang and 1 more

Open access · greenAbstract read
In one paragraph

Article in Cellular & molecular immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
7.1field-weighted citation impact, top 2% 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

46 citing papers in PubMed, 86 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

11 authors at 3 institutions in 1 country.

Bo ZengDepartment of Clinical Laboratory, The Fifth Affiliated Hospital of Jinan University, Heyuan, China.
Yuanting HuangDepartment of Immunobiology, College of Life Science and Technology, Jinan University, Guangzhou, China.
Siyuan ChenDepartment of Immunobiology, College of Life Science and Technology, Jinan University, Guangzhou, China.
Rong XuDepartment of Immunobiology, College of Life Science and Technology, Jinan University, Guangzhou, China.
Lihui XuDepartment of Cell Biology, College of Life Science and Technology, Jinan University, Guangzhou, China.
Jiahao QiuDepartment of Immunobiology, College of Life Science and Technology, Jinan University, Guangzhou, China.
Fuli ShiDepartment of Immunobiology, College of Life Science and Technology, Jinan University, Guangzhou, China.
Siying LiuDepartment of Immunobiology, College of Life Science and Technology, Jinan University, Guangzhou, China.
Qingbing ZhaDepartment of Clinical Laboratory, The Fifth Affiliated Hospital of Jinan University, Heyuan, China. zhaqingbb@sina.com.
Dongyun OuyangDepartment of Immunobiology, College of Life Science and Technology, Jinan University, Guangzhou, China. dongyun1967@aliyun.com.
Xianhui HeDepartment of Clinical Laboratory, The Fifth Affiliated Hospital of Jinan University, Heyuan, China. thexh@jnu.edu.cn.ORCID http://orcid.org/0000-0001-7433-7392
Jinan University · CNHarbin Medical University · CNXinjiang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammatory bowel disease (IBD), including Crohn's disease and ulcerative colitis, has increased in incidence and prevalence in recent decades. Both clinical and animal studies are critical for understanding the pathogenesis of this disease. Dextran sodium sulfate (DSS)-induced colitis is a frequently used animal model of IBD, but the underlying mechanism of the model remains incompletely understood. In this study, we found that NOD-like receptor family pyrin containing 3 (NLRP3) depletion markedly mitigated DSS-induced colitis and was accompanied by decreased activation of the inflammasome in the colons of mice. However, in vitro assays showed that DSS did not directly trigger but instead potentiated NLRP3 inflammasome assembly in macrophages in response to suboptimal ATP or nigericin stimulation. Mechanistically, DSS potentiated NLRP3 inflammasome activation in macrophages by augmenting KCa3.1-mediated potassium ion (K

Indexed as

ColitisInflammatory Bowel DiseasesAnimalsDextran SulfateDisease Models, AnimalInflammasomesIntermediate-Conductance Calcium-Activated Potassium ChannelsMiceMice, Inbred C57BLNLR Family, Pyrin Domain-Containing 3 ProteinPotassium ChannelsSulfatesDextran SulfateInflammasomesIntermediate-Conductance Calcium-Activated Potassium ChannelsKcnn4 protein, mouseNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mousePotassium Channelssodium sulfateSulfatesDextran sodium sulfateInflammasomeInflammatory bowel diseaseKCa3.1Potassium ion channelTRAM-34.

Identifiers

PMID35799057
PMCPMC9338299
OpenAlexW4284882930

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.