Evidence map›Paper›PMID 26467446›Full record

ArticleInfection and immunity2016

Pseudomonas aeruginosa Triggers Macrophage Autophagy To Escape Intracellular Killing by Activation of the NLRP3 Inflammasome.

Qiuchan Deng, Yi Wang, Yuanqing Zhang, Meiyu Li, Dandan Li, Xi Huang, Yongjian Wu, Jieying Pu, Minhao Wu

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

71 citing papers in PubMed, 115 citations in OpenAlex.

  1. Article
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  7. Review
  8. Management Strategies for Chronic Suppurative Otitis Media and Why They Fail.Journal of the Association for Research in Otolaryngology : JARO · 2025
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  9. EpithelialMedComm · 2025
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  13. Evidence for intracellularJournal of bacteriology · 2024
    Review
  14. Article
  15. AFM41a: A Novel PAD2 Inhibitor for Sepsis Treatment-Efficacy and Mechanism.International journal of biological sciences · 2024
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

11 more citing papers are in PubMed but not listed here.

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.

Qiuchan DengDepartment of Immunology, Zhongshan School of Medicine, Institute of Human Virology, Institute of Tuberculosis Control, Sun Yat-sen University, Guangzhou, China Key Laboratory of Tropical Diseases Control (Sun Yat-sen University), Ministry of Education, Guangzhou, China.
Yi WangDepartment of Immunology, Zhongshan School of Medicine, Institute of Human Virology, Institute of Tuberculosis Control, Sun Yat-sen University, Guangzhou, China Key Laboratory of Tropical Diseases Control (Sun Yat-sen University), Ministry of Education, Guangzhou, China.
Yuanqing ZhangSchool of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou, China.
Meiyu LiDepartment of Immunology, Zhongshan School of Medicine, Institute of Human Virology, Institute of Tuberculosis Control, Sun Yat-sen University, Guangzhou, China Key Laboratory of Tropical Diseases Control (Sun Yat-sen University), Ministry of Education, Guangzhou, China.
Dandan LiDepartment of Immunology, Zhongshan School of Medicine, Institute of Human Virology, Institute of Tuberculosis Control, Sun Yat-sen University, Guangzhou, China Key Laboratory of Tropical Diseases Control (Sun Yat-sen University), Ministry of Education, Guangzhou, China.
Xi HuangDepartment of Immunology, Zhongshan School of Medicine, Institute of Human Virology, Institute of Tuberculosis Control, Sun Yat-sen University, Guangzhou, China Key Laboratory of Tropical Diseases Control (Sun Yat-sen University), Ministry of Education, Guangzhou, China.
Yongjian WuDepartment of Immunology, Zhongshan School of Medicine, Institute of Human Virology, Institute of Tuberculosis Control, Sun Yat-sen University, Guangzhou, China Key Laboratory of Tropical Diseases Control (Sun Yat-sen University), Ministry of Education, Guangzhou, China.
Jieying PuDepartment of Immunology, Zhongshan School of Medicine, Institute of Human Virology, Institute of Tuberculosis Control, Sun Yat-sen University, Guangzhou, China Key Laboratory of Tropical Diseases Control (Sun Yat-sen University), Ministry of Education, Guangzhou, China.
Minhao WuDepartment of Immunology, Zhongshan School of Medicine, Institute of Human Virology, Institute of Tuberculosis Control, Sun Yat-sen University, Guangzhou, China Key Laboratory of Tropical Diseases Control (Sun Yat-sen University), Ministry of Education, Guangzhou, China wuminhao@mail.sysu.edu.cn.
Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Assembly of the inflammasome has recently been identified to be a critical event in the initiation of inflammation. However, its role in bacterial killing remains unclear. Our study demonstrates that Pseudomonas aeruginosa infection induces the assembly of the NLRP3 inflammasome and the sequential secretion of caspase1 and interleukin-1β (IL-1β) in human macrophages. More importantly, activation of the NLRP3 inflammasome reduces the killing of P. aeruginosa in human macrophages, without affecting the generation of antimicrobial peptides, reactive oxygen species, and nitric oxide. In addition, our results demonstrate that P. aeruginosa infection increases the amount of the LC3-II protein and triggers the formation of autophagosomes in human macrophages. The P. aeruginosa-induced autophagy was enhanced by overexpression of NLRP3, ASC, or caspase1 but was reduced by knockdown of these core molecules of the NLRP3 inflammasome. Treatment with IL-1β enhanced autophagy in human macrophages. More importantly, IL-1β decreased the macrophage-mediated killing of P. aeruginosa, whereas knockdown of ATG7 or Beclin1 restored the IL-1β-mediated suppression of bacterial killing. Collectively, our study explores a novel mechanism employed by P. aeruginosa to escape from phagocyte killing and may provide a better understanding of the interaction between P. aeruginosa and host immune cells, including macrophages.

Indexed as

AdultApoptosis Regulatory ProteinsAutophagyAutophagy-Related Protein 7Beclin-1CARD Signaling Adaptor ProteinsCarrier ProteinsCaspase 1Cell LineCytoskeletal ProteinsFemaleHumansInflammationInterleukin-1betaMacrophagesMaleApoptosis Regulatory ProteinsATG7 protein, humanAutophagy-Related Protein 7Beclin-1BECN1 protein, humanCARD Signaling Adaptor ProteinsCarrier ProteinsCaspase 1Cytoskeletal ProteinsIL1B protein, humanInterleukin-1betaMAP1LC3A protein, humanMembrane ProteinsMicrotubule-Associated ProteinsNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mousePYCARD protein, humanRNA, Small InterferingUbiquitin-Activating Enzymes

Identifiers

PMID26467446
PMCPMC4694000
OpenAlexW2221571272

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.