Evidence map›Paper›PMID 27458013›Full record

ArticleThe Journal of biological chemistry2016

Mycotoxin Patulin Suppresses Innate Immune Responses by Mitochondrial Dysfunction and p62/Sequestosome-1-dependent Mitophagy.

Wan-Ting Tsai, Yin-Chiu Lo, Ming-Sian Wu, Chia-Yang Li, Yi-Ping Kuo, Yi-Hui Lai, Yu Tsai, Kai-Chieh Chen, Tsung-Hsien Chuang, Chun-Hsu Yao and 4 more

Abstract read
In one paragraph

Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–field-weighted citation impact
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

22 citing papers in PubMed.

  1. Review
  2. Article
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  6. Review
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  10. Article
  11. Article
  12. Fungal Toxins and Host Immune Responses.Frontiers in microbiology · 2021
    Review
  13. Article
  14. Article
  15. Patulin suppresses αScientific reports · 2020
    Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review
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

14 authors.

Wan-Ting TsaiFrom the National Institute of Infectious Diseases and Vaccinology.
Yin-Chiu LoFrom the National Institute of Infectious Diseases and Vaccinology.
Ming-Sian WuFrom the National Institute of Infectious Diseases and Vaccinology.
Chia-Yang LiFrom the National Institute of Infectious Diseases and Vaccinology, the Department of Genome Medicine, College of Medicine, and Center for Infectious Disease and Cancer Research, Kaohsiung Medical University, Kaohsiung 80708, Taiwan.
Yi-Ping KuoFrom the National Institute of Infectious Diseases and Vaccinology.
Yi-Hui Laithe Institute of Molecular Medicine, College of Medicine, National Taiwan University, Taipei 10002, Taiwan, and.
Yu TsaiFrom the National Institute of Infectious Diseases and Vaccinology.
Kai-Chieh ChenFrom the National Institute of Infectious Diseases and Vaccinology.
Tsung-Hsien ChuangImmunology Research Center, and.
Chun-Hsu YaoInstitute of Biotechnology and Pharmaceutical Research, National Health Research Institutes, Zhunan Town, Miaoli County 35053, Taiwan.
Jinq-Chyi LeeInstitute of Biotechnology and Pharmaceutical Research, National Health Research Institutes, Zhunan Town, Miaoli County 35053, Taiwan.
Li-Chung Hsuthe Institute of Molecular Medicine, College of Medicine, National Taiwan University, Taipei 10002, Taiwan, and.
John T-A HsuInstitute of Biotechnology and Pharmaceutical Research, National Health Research Institutes, Zhunan Town, Miaoli County 35053, Taiwan.
Guann-Yi YuFrom the National Institute of Infectious Diseases and Vaccinology, the Center of Infectious Disease and Signaling Research, National Cheng-Kung University, Tainan 70101, Taiwan guannyiy@nhri.org.tw.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Innate immune responses are important for pathogen elimination and adaptive immune response activation. However, excess inflammation may contribute to immunopathology and disease progression (e.g. inflammation-associated hepatocellular carcinoma). Immune modulation resulting from pattern recognition receptor-induced responses is a potential strategy for controlling immunopathology and related diseases. This study demonstrates that the mycotoxin patulin suppresses Toll-like receptor- and RIG-I/MAVS-dependent cytokine production through GSH depletion, mitochondrial dysfunction, the activation of p62-associated mitophagy, and p62-TRAF6 interaction. Blockade of autophagy restored the immunosuppressive activity of patulin, and pharmacological activation of p62-dependent mitophagy directly reduced RIG-I-like receptor-dependent inflammatory cytokine production. These results demonstrated that p62-dependent mitophagy has an immunosuppressive role to innate immune response and might serve as a potential immunomodulatory target for inflammation-associated diseases.

Indexed as

AnimalsHEK293 CellsHumansImmunity, InnateMiceMitophagyMycotoxinsPatulinRAW 264.7 CellsSequestosome-1 ProteinMycotoxinsPatulinSequestosome-1 ProteinSQSTM1 protein, humanSqstm1 protein, mouseimmunomodulationmitochondriamitophagymycotoxinp62 (sequestosome 1(SQSTM1))patulinRIG-I-like receptor (RLR)toll-like receptor (TLR)

Identifiers

PMID27458013
PMCPMC5016671

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.