Evidence map›Paper›PMID 27159636›Full record

ArticleAutophagy2016

Pseudomonas toxin pyocyanin triggers autophagy: Implications for pathoadaptive mutations.

Zhong-Shan Yang, Lan-Qing Ma, Kun Zhu, Jin-Yuan Yan, Li Bian, Ke-Qin Zhang, Cheng-Gang Zou

Abstract read
In one paragraph

Article in Autophagy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

24 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  9. Review
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  15. Bacterial Subversion of Autophagy in Cystic Fibrosis.Frontiers in cellular and infection microbiology · 2021
    Review
  16. Review
  17. The integrated stress response in pulmonary disease.European respiratory review : an official journal of the European Respiratory Society · 2020
    Review
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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.

Zhong-Shan Yanga Key State Laboratory for Conservation and Utilization of Bio-Resources in Yunnan, Yunnan University , Kunming , Yunnan , China.
Lan-Qing Mac Yunnan Institute of Digestive Disease, Department of Digestive Diseases, The First Affiliated Hospital, Kunming Medical University , Kunming , Yunnan , China.
Kun Zhud Institute of Microbiology, Chinese Academy of Science , Beijing , China.
Jin-Yuan Yana Key State Laboratory for Conservation and Utilization of Bio-Resources in Yunnan, Yunnan University , Kunming , Yunnan , China.
Li Biane Department of Pathology , The First Affiliated Hospital, Kunming Medical University , Kunming , Yunnan , China.
Ke-Qin Zhanga Key State Laboratory for Conservation and Utilization of Bio-Resources in Yunnan, Yunnan University , Kunming , Yunnan , China.
Cheng-Gang Zoua Key State Laboratory for Conservation and Utilization of Bio-Resources in Yunnan, Yunnan University , Kunming , Yunnan , China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pseudomonas aeruginosa can establish life-long chronic infection in patients with cystic fibrosis by generating genetic loss-of-function mutations, which enhance fitness of the bacterium in the airways. However, the precise role of the pathoadaptive mutations in persistence in chronic airways infection remains largely unknown. Here we demonstrate that pyocyanin, a well-described P. aeruginosa virulence factor that plays an important role in the initial infection, promotes autophagy in bronchial epithelial cells. Disruption of phzM, which is required for pyocyanin biosynthesis, leads to a significant reduction in autophagy in Beas-2B cells and lung tissues. Pyocyanin-induced autophagy is mediated by the EIF2AK4/GCN2-EIF2S1/eIF2α-ATF4 pathway. Interestingly, rats infected with the phzMΔ mutant strain have high mortality rate and numbers of colony-forming units, compared to those infected with wild-type (WT) P. aeruginosa PA14 strain, during chronic P. aeruginosa infection. In addition, the phzMΔ mutant strain induces more extensive alveolar wall thickening than the WT strain in the pulmonary airways of rats. As autophagy plays an essential role in suppressing bacterial burden, our findings provide a detailed understanding of why reduction of pyocyanin production in P. aeruginosa in chronic airways infections has been associated with better host adaptation and worse outcomes in cystic fibrosis.

Indexed as

Adaptation, PhysiologicalAnimalsAutophagosomesAutophagyBacterial ToxinsBronchiChronic DiseaseEpithelial CellsHumansInflammationMutationPneumoniaPseudomonasPseudomonas InfectionsPyocyanineRats, Sprague-DawleyBacterial ToxinsPyocyanineautophagyEIF2AK4/GCN2lungpathoadaptive mutationsPseudomonas aeruginosapyocyanin

Identifiers

PMID27159636
PMCPMC4922443

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.