Evidence map›Paper›PMID 35173714›Full record

ArticleFrontiers in immunology2022

All-Trans Retinoic Acid Attenuates Transmissible Gastroenteritis Virus-Induced Inflammation in IPEC-J2 Cells

Junning Pu, Daiwen Chen, Gang Tian, Jun He, Zhiqing Huang, Ping Zheng, Xiangbing Mao, Jie Yu, Junqiu Luo, Yuheng Luo and 2 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 7% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. [Effects and mechanism of retinoic acid on radiation-induced skin injury in mice].Zhonghua shao shang yu chuang mian xiu fu za zhi · 2025
    Article
  7. Retinoic acid ameliorates rheumatoid arthritis by attenuating inflammation and modulating macrophage polarization through MKP-1/MAPK signaling pathway.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
    Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article
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

12 authors at 1 institution in 1 country.

Junning PuKey Laboratory for Animal Disease-Resistance Nutrition, Ministry of Education/Institute of Animal Nutrition, Sichuan Agricultural University, Chengdu, China.
Daiwen ChenKey Laboratory for Animal Disease-Resistance Nutrition, Ministry of Education/Institute of Animal Nutrition, Sichuan Agricultural University, Chengdu, China.
Gang TianKey Laboratory for Animal Disease-Resistance Nutrition, Ministry of Education/Institute of Animal Nutrition, Sichuan Agricultural University, Chengdu, China.
Jun HeKey Laboratory for Animal Disease-Resistance Nutrition, Ministry of Education/Institute of Animal Nutrition, Sichuan Agricultural University, Chengdu, China.
Zhiqing HuangKey Laboratory for Animal Disease-Resistance Nutrition, Ministry of Education/Institute of Animal Nutrition, Sichuan Agricultural University, Chengdu, China.
Ping ZhengKey Laboratory for Animal Disease-Resistance Nutrition, Ministry of Education/Institute of Animal Nutrition, Sichuan Agricultural University, Chengdu, China.
Xiangbing MaoKey Laboratory for Animal Disease-Resistance Nutrition, Ministry of Education/Institute of Animal Nutrition, Sichuan Agricultural University, Chengdu, China.
Jie YuKey Laboratory for Animal Disease-Resistance Nutrition, Ministry of Education/Institute of Animal Nutrition, Sichuan Agricultural University, Chengdu, China.
Junqiu LuoKey Laboratory for Animal Disease-Resistance Nutrition, Ministry of Education/Institute of Animal Nutrition, Sichuan Agricultural University, Chengdu, China.
Yuheng LuoKey Laboratory for Animal Disease-Resistance Nutrition, Ministry of Education/Institute of Animal Nutrition, Sichuan Agricultural University, Chengdu, China.
Hui YanKey Laboratory for Animal Disease-Resistance Nutrition, Ministry of Education/Institute of Animal Nutrition, Sichuan Agricultural University, Chengdu, China.
Bing YuKey Laboratory for Animal Disease-Resistance Nutrition, Ministry of Education/Institute of Animal Nutrition, Sichuan Agricultural University, Chengdu, China.
Sichuan Agricultural University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transmissible gastroenteritis virus (TGEV) infection can cause transmissible gastroenteritis (TGE), especially in suckling piglets, resulting in a significant economic loss for the global pig industry. The pathogenesis of TGEV infection is closely related to intestinal inflammation. All-trans retinoic acid (ATRA) has anti-inflammatory activity and immunomodulatory properties, but it is unclear whether ATRA can attenuate the inflammatory response induced by TGEV. This study aimed to investigate the protective effect of ATRA on TGEV-induced inflammatory injury in intestinal porcine epithelial cells (IPEC-J2) and to explore the underlying molecular mechanism. The results showed that TGEV infection triggered inflammatory response and damaged epithelial barrier integrity in IPEC-J2 cells. However, ATRA attenuated TGEV-induced inflammatory response by inhibiting the release of pro-inflammatory cytokines, including IL-1β, IL-6, IL-8 and TNF-α. ATRA also significantly reversed the reduction of ZO-1 and Occludin protein levels induced by TGEV infection and maintained epithelial barrier integrity. Moreover, ATRA treatment significantly prevented the upregulation of IкBα and NF-κB p65 phosphorylation levels and the nuclear translocation of NF-кB p65 induced by TGEV. On the other hand, treatment of TGEV-infected IPEC-J2 cells with the NF-κB inhibitors (BAY11-7082) significantly decreased the levels of inflammatory cytokines. Furthermore, ATRA treatment significantly downregulated the mRNA abundance and protein levels of TLR3, TLR7, RIG-I and MDA5, and downregulated their downstream signaling molecules

Indexed as

AnimalsCell LineCytokinesDown-RegulationGastroenteritis, Transmissible, of SwineInflammationNF-kappa BPhosphorylationSignal TransductionSwineTranscription Factor RelATransmissible gastroenteritis virusTretinoinTumor Necrosis Factor-alphaCytokinesNF-kappa BTranscription Factor RelATretinoinTumor Necrosis Factor-alphaall-trans retinoic acidinflammationIPEC-J2 cells damageRLRs/NF‐κB pathwaytransmissible gastroenteritis virus

Identifiers

PMID35173714
PMCPMC8841732
OpenAlexW4210616638

What OpenQuestion holds

Textmetadata
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.