Evidence map›Paper›PMID 31997584›Full record

ArticleJournal of cellular and molecular medicine2020

Staphylococcus aureus facilitates its survival in bovine macrophages by blocking autophagic flux.

Juan Cai, Jun Li, Yuqi Zhou, Jianqiang Wang, Jianji Li, Luying Cui, Xia Meng, Guoqiang Zhu, Heng Wang

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

34 citing papers in PubMed, 54 citations in OpenAlex.

  1. An underlying mechanism of bovine mastitis: PGEThe veterinary quarterly · 2026
    Article
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  3. Intracellular survival ofVirulence · 2025
    Review
  4. Strategies for Survival ofInternational journal of molecular sciences · 2025
    Review
  5. Review
  6. Article
  7. Autophagy reports · 2025
    Article
  8. Article
  9. Staphylococcal mastitis in dairy cows.Frontiers in veterinary science · 2024
    Review
  10. Complement C3 deposition restricts the proliferation of internalizedFrontiers in cellular and infection microbiology · 2024
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Rapamycin ExacerbatesJournal of inflammation research · 2023
    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

9 authors at 1 institution in 1 country.

Juan CaiCollege of Veterinary Medicine, Yangzhou University, Yangzhou, China.ORCID 0000-0001-6700-0310
Jun LiCollege of Veterinary Medicine, Yangzhou University, Yangzhou, China.
Yuqi ZhouCollege of Veterinary Medicine, Yangzhou University, Yangzhou, China.
Jianqiang WangCollege of Veterinary Medicine, Yangzhou University, Yangzhou, China.
Jianji LiCollege of Veterinary Medicine, Yangzhou University, Yangzhou, China.
Luying CuiCollege of Veterinary Medicine, Yangzhou University, Yangzhou, China.
Xia MengCollege of Veterinary Medicine, Yangzhou University, Yangzhou, China.
Guoqiang ZhuCollege of Veterinary Medicine, Yangzhou University, Yangzhou, China.
Heng WangCollege of Veterinary Medicine, Yangzhou University, Yangzhou, China.
Yangzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Staphylococcus aureus is a pathogen that is the causative agent of several human and veterinary infections and plays a critical role in the clinical and subclinical mastitis of cattle. Autophagy is a conserved pathogen defence mechanism in eukaryotes. Studies have reported that S aureus can subvert autophagy and survive in cells. Staphylococcus aureus survival in cells is an important cause of chronic persistent mastitis infection. However, it is unclear whether S aureus can escape autophagy in innate immune cells. In this study, initiation of autophagy due to the presence of S aureus was detected in bovine macrophages. We observed autophagic vacuoles increased after S aureus infection of bovine macrophages by transmission electron microscopy (TEM). It was also found that S aureus-infected bovine macrophages increased the expression of LC3 at different times(0, 0.5, 1, 1.5, 2, 2.5, 3 and 4 hours). Data also showed the accumulation of p62 induced by S aureus infection. Application of autophagy regulatory agents showed that the degradation of p62 was blocked in S aureus induced bovine macrophages. In addition, we also found that the accumulation of autophagosomes promotes S aureus to survive in macrophage cells. In conclusion, this study indicates that autophagy occurs in S aureus-infected bovine macrophages but is blocked at a later stage of autophagy. The accumulation of autophagosomes facilitates the survival of S aureus in bovine macrophages. These findings provide new insights into the interaction of S aureus with autophagy in bovine macrophages.

Indexed as

AnimalsAutophagosomesAutophagyCattleCell LineFemaleMacrophagesMastitis, BovineMicrotubule-Associated ProteinsReceptors, ImmunologicStaphylococcal InfectionsStaphylococcus aureusMicrotubule-Associated Proteinsp62 natural killer cell receptorReceptors, Immunologicautophagybovine macrophageStaphylococcus aureus

Identifiers

PMID31997584
PMCPMC7131951
OpenAlexW3003420934

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.