Evidence map›Paper›PMID 35233679›Full record

ArticleMolecular biology reports2022

The toxicity of perfluorodecanoic acid is mainly manifested as a deflected immune function.

Keming Li, Qian Zhao, Ziyan Fan, Shouyin Jia, Qing Liu, Fengyan Liu, Shili Liu

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular biology reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.2field-weighted citation impact, top 25% 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

3 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. 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

7 authors at 4 institutions in 1 country.

Keming Li *Department of Medical Microbiology, School of Basic Medical Science & Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250012, Shandong, China.
Qian Zhao *Department of Medical Microbiology, School of Basic Medical Science & Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250012, Shandong, China.
Ziyan Fan *China National Tobacco Quality Supervision and Test Center, Zhengzhou, 450001, Henan, China.
Shouyin JiaDepartment of Medical Microbiology, School of Basic Medical Science & Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250012, Shandong, China.
Qing LiuShandong Provincial Hospital affiliated to Shandong First Medical University, Jinan, 250021, Shandong, China.
Fengyan LiuThe Second Hospital of Shandong University, Jinan, 250012, Shandong, China.
Shili LiuDepartment of Medical Microbiology, School of Basic Medical Science & Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250012, Shandong, China. liushili@sdu.edu.cn.ORCID http://orcid.org/0000-0003-3314-7749
Shandong University · CNChina Tobacco · CNSecond Hospital of Shandong University · CNShandong Provincial Hospital · CN

Funding

Natural Science Foundation of Shandong Province ZR2020QH220open research fund of state key laboratory of environmental chemistry and ecotoxicology KF2014-08
6 · The paper itself

Abstract

backgroundPerfluorodecanoic acid (PFDA) is a type of perfluoroalkyl acid (PFAA). PFDA has toxicity similar to dioxin; its effect on the body is not through a single target or a single pathway. However, the mechanism at the global level is still unclear. METHODS AND

resultsWe treated mice with PFDA and characterized the global changes in gene expression in the liver using microarray analyses. The enriched KEGG pathways and GO analyses revealed that PFDA greatly affected the immune response, which was different from the response of gastric cells previously studied. As a proof of principle, the expressions of IL-1β and IL-18 were both decreased after PFDA treatment, and qRT-PCR and ELISAs verified the reduction of IL-1β and IL-18 in liver tissues. Mechanistic investigations indicated that PFDA inhibited caspase-1 activation, and decreased the mRNA levels of NLRP1, NLRP3, and NLRC4; thus, suggesting that inflammasome assemblies were suppressed. Further microarray data revealed that cIAP2 and its binding proteins, which are critical for regulating inflammasome assembly, were also repressed by PFDA. In addition, flow cytometry results revealed a significant inhibition of Th1 cell differentiation in the livers of PFDA-treated mice.

conclusionsThe results of this study suggested that one of the main toxic effects of PFDA on livers was the inhibition of immune response.

Indexed as

FluorocarbonsAnimalsDecanoic AcidsImmunityInflammasomesInterleukin-18Interleukin-1betaMiceDecanoic AcidsFluorocarbonsInflammasomesInterleukin-18Interleukin-1betaperfluorodecanoic acidcIAP2Immune responsesInflammasomesPFDATh1

Identifiers

PMID35233679
OpenAlexW4214831109

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.