Evidence map›Paper›PMID 28558839›Full record

ArticleParasites & vectors2017

NLRP3 inflammasome activation in murine macrophages caused by Neospora caninum infection.

Xiaocen Wang, Pengtao Gong, Xu Zhang, Jielin Wang, Lixin Tai, Xu Wang, Zhengkai Wei, Yongjun Yang, Zhengtao Yang, Jianhua Li and 1 more

Open access · goldAbstract read
In one paragraph

Article in Parasites & vectors, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.0field-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

28 citing papers in PubMed, 46 citations in OpenAlex.

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  13. Nucleotide receptors mediate protection against neonatal sepsis and meningitis caused by alpha-hemolysin expressing Escherichia coli K1.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
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  14. Frontiers in immunology · 2022
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  16. Frontiers in cellular and infection microbiology · 2021
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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 1 institution in 1 country.

Xiaocen WangCollege of Veterinary Medicine, Jilin University, Jilin, Changchun, 130062, China.
Pengtao GongCollege of Veterinary Medicine, Jilin University, Jilin, Changchun, 130062, China.
Xu ZhangCollege of Veterinary Medicine, Jilin University, Jilin, Changchun, 130062, China.
Jielin WangCollege of Veterinary Medicine, Jilin University, Jilin, Changchun, 130062, China.
Lixin TaiCollege of Veterinary Medicine, Jilin University, Jilin, Changchun, 130062, China.
Xu WangCollege of Veterinary Medicine, Jilin University, Jilin, Changchun, 130062, China.
Zhengkai WeiCollege of Veterinary Medicine, Jilin University, Jilin, Changchun, 130062, China.
Yongjun YangCollege of Veterinary Medicine, Jilin University, Jilin, Changchun, 130062, China.
Zhengtao YangCollege of Veterinary Medicine, Jilin University, Jilin, Changchun, 130062, China.
Jianhua LiCollege of Veterinary Medicine, Jilin University, Jilin, Changchun, 130062, China. jianhuali7207@163.com.
Xichen ZhangCollege of Veterinary Medicine, Jilin University, Jilin, Changchun, 130062, China. xczhang@jlu.edu.cn.
Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNeospora caninum is an intracellular parasite that causes significant economic losses in cattle industry. Understanding the host resistance mechanisms in the innate immune response to neosporosis could facilitate the exploration of approaches for controlling N. caninum infection. The NLR inflammasome is a multiprotein platform in the cell cytoplasm and plays critical roles in the host response against microbes.

methodsNeospora caninum-infected wild-type (WT) macrophages and Nlrp3

resultsMany NLR molecules participated in the recognition of N. caninum, especially the sensor protein NLRP3, and further study revealed that the NLRP3 distribution became punctate in the cell cytoplasm, which facilitated inflammasome activation. Inflammasome activation-mediated caspase-1 processing and IL-1β cleavage in response to N. caninum infection were observed and were correlated with the time of infection and number of infecting parasites. LDH-related cell death was also observed, and this death was regarded as beneficial for the clearance of N. caninum. Treatment of N. caninum-infected macrophages with caspase-1, pan-caspase and NLRP3 inhibitors led to the impaired release of active IL-1β and a failure to restrict parasite replication. And Neospora caninum infected peritoneal macrophages from Nlrp3-deficient mice displayed greatly decreased release of active IL-1β and the failure of caspase-1 cleavage.

conclusionsThe NLRP3 inflammasome can be activated in N. caninum-infected macrophages, and plays a protective role in the host response to control N. caninum.

Indexed as

AnimalsCaspase 1CattleCattle DiseasesCoccidiosisFemaleInflammasomesInterleukin-1betaMacrophagesMiceMice, Inbred C57BLNeosporaNLR Family, Pyrin Domain-Containing 3 ProteinCaspase 1InflammasomesInterleukin-1betaNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseCaspase-1IL-1βMacrophagesNeospora caninumNLRP3 inflammasome

Identifiers

PMID28558839
PMCPMC5450200
OpenAlexW2617157549

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.