Evidence map›Paper›PMID 28504245›Full record

ArticleCellular & molecular immunology2018

Macrophage-derived IL-1α promotes sterile inflammation in a mouse model of acetaminophen hepatotoxicity.

Chao Zhang, Jin Feng, Jun Du, Zhiyong Zhuo, Shuo Yang, Weihong Zhang, Weihong Wang, Shengyuan Zhang, Yoichiro Iwakura, Guangxun Meng and 3 more

Abstract read
In one paragraph

Article in Cellular & molecular immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
10.7field-weighted citation impact, top 1% 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

58 citing papers in PubMed, 100 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Liver macrophages: development, dynamics, and functions.Cellular & molecular immunology · 2025
    Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. TLR9-independent CD8Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 5 institutions in 3 countries.

Chao ZhangThe Key Laboratory of Infection and Immunity, The Institute of Biophysics, Chinese Academy of Sciences, 100101, Beijing, China.
Jin FengThe Key Laboratory of Infection and Immunity, The Institute of Biophysics, Chinese Academy of Sciences, 100101, Beijing, China.
Jun DuThe Institute of Biotechnology, Shanxi University, 030006, Taiyuan, China.
Zhiyong ZhuoThe Key Laboratory of Infection and Immunity, The Institute of Biophysics, Chinese Academy of Sciences, 100101, Beijing, China.
Shuo YangThe Key Laboratory of Infection and Immunity, The Institute of Biophysics, Chinese Academy of Sciences, 100101, Beijing, China.
Weihong ZhangThe Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences, 200031, Shanghai, China.
Weihong WangThe Key Laboratory of Infection and Immunity, The Institute of Biophysics, Chinese Academy of Sciences, 100101, Beijing, China.
Shengyuan ZhangThe Key Laboratory of Infection and Immunity, The Institute of Biophysics, Chinese Academy of Sciences, 100101, Beijing, China.
Yoichiro IwakuraDivision of Experimental Animal Immunology, Center for Animal Disease Models, Research Institute for Biomedical Sciences, Tokyo University of Science, 278-0022, Chiba, Japan.
Guangxun MengThe Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences, 200031, Shanghai, China.
Yang-Xin FuThe Key Laboratory of Infection and Immunity, The Institute of Biophysics, Chinese Academy of Sciences, 100101, Beijing, China.
Baidong HouThe Key Laboratory of Infection and Immunity, The Institute of Biophysics, Chinese Academy of Sciences, 100101, Beijing, China.
Hong TangThe Key Laboratory of Infection and Immunity, The Institute of Biophysics, Chinese Academy of Sciences, 100101, Beijing, China. htang@ips.ac.cn.
Chinese Academy of Sciences · CNInstitute of Biophysics · CNInstitut Pasteur of Shanghai · CNShanxi University · CNTokyo University of Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The metabolic intermediate of acetaminophen (APAP) can cause severe hepatocyte necrosis, which triggers aberrant immune activation of liver non-parenchymal cells (NPC). Overzealous hepatic inflammation determines the morbidity and mortality of APAP-induced liver injury (AILI). Interleukin-1 receptor (IL-1R) signaling has been shown to play a critical role in various inflammatory conditions, but its precise role and underlying mechanism in AILI remain debatable. Herein, we show that NLRP3 inflammasome activation of IL-1β is dispensable to AILI, whereas IL-1α, the other ligand of IL-1R1, accounts for hepatic injury by a lethal dose of APAP. Furthermore, Kupffer cells function as a major source of activated IL-1α in the liver, which is activated by damaged hepatocytes through TLR4/MyD88 signaling. Finally, IL-1α is able to chemoattract and activate CD11b

Indexed as

AcetaminophenAnimalsChemical and Drug Induced Liver InjuryDisease Models, AnimalInflammationInterleukin-1alphaKupffer CellsMiceMice, KnockoutMyeloid Differentiation Factor 88Receptors, Interleukin-1 Type ISignal TransductionAcetaminophenIL1R1 protein, mouseInterleukin-1alphaMyd88 protein, mouseMyeloid Differentiation Factor 88Receptors, Interleukin-1 Type IacetaminophenIL-αKupffer cellssterile immunityTLR4

Identifiers

PMID28504245
PMCPMC6207754
OpenAlexW2616675556

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.