Evidence map›Paper›PMID 27046446›Full record

ArticleScientific reports2016

Adh enhances Actinobacillus pleuropneumoniae pathogenicity by binding to OR5M11 and activating p38 which induces apoptosis of PAMs and IL-8 release.

Lei Wang, Wanhai Qin, Jing Zhang, Chuntong Bao, Hu Zhang, Yanyi Che, Changjiang Sun, Jingmin Gu, Xin Feng, Chongtao Du and 3 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
4.1field-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

13 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Naringin's Alleviation of the Inflammatory Response Caused byInternational journal of molecular sciences · 2024
    Article
  5. Adh PromotesCells · 2023
    Article
  6. Article
  7. Frontiers in veterinary science · 2020
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. 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

13 authors at 3 institutions in 2 countries.

Lei WangCollege of Veterinary Medicine, JiLin University, Changchun, P. R. China.
Wanhai QinCollege of Veterinary Medicine, JiLin University, Changchun, P. R. China.
Jing ZhangChangchun University of Chinese Medicine, Changchun, P. R. China.
Chuntong BaoCollege of Veterinary Medicine, JiLin University, Changchun, P. R. China.
Hu ZhangCollege of Veterinary Medicine, JiLin University, Changchun, P. R. China.
Yanyi CheCollege of Veterinary Medicine, JiLin University, Changchun, P. R. China.
Changjiang SunCollege of Veterinary Medicine, JiLin University, Changchun, P. R. China.
Jingmin GuCollege of Veterinary Medicine, JiLin University, Changchun, P. R. China.
Xin FengCollege of Veterinary Medicine, JiLin University, Changchun, P. R. China.
Chongtao DuCollege of Veterinary Medicine, JiLin University, Changchun, P. R. China.
Wenyu HanCollege of Veterinary Medicine, JiLin University, Changchun, P. R. China.
Paul Langford RichardSection of Paediatrics, Imperial College London, London, UK.
Liancheng LeiCollege of Veterinary Medicine, JiLin University, Changchun, P. R. China.
Jilin University · CNChangchun University of Chinese Medicine · CNImperial College London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Members of the Trimeric Autotransporter Adhesin (TAA) family play a crucial role in the adhesion of Gram-negative pathogens to host cells, but the immunopathogenesis of TAAs remains unknown. Our previous studies demonstrated that Adh from Actinobacillus pleuropneumoniae (A. pleuropneumoniae) is required for full bacterial pathogenicity. Alveolar macrophages are the first line of defense against respiratory infections. This study compared the interactions between porcine alveolar macrophages (PAMs) and wild-type A. pleuropneumoniae (5b WT) or an Adh-deletion strain (5b ΔAdh) via gene microarray, immunoprecipitation and other technologies. We found that Adh was shown to interact with the PAMs membrane protein OR5M11, an olfactory receptor, resulting in the high-level secretion of IL-8 by activation of p38 MAPK signaling pathway. Subsequently, PAMs apoptosis via the activation of the Fax and Bax signaling pathways was observed, followed by activation of caspases 8, 9, and 3. The immunological pathogenic roles of Adh were also confirmed in both murine and piglets infectious models in vivo. These results identify a novel immunological strategy for TAAs to boost the pathogenicity of A. pleuropneumoniae. Together, these datas reveal the high versatility of the Adh protein as a virulence factor and provide novel insight into the immunological pathogenic role of TAAs.

Indexed as

ApoptosisActinobacillus pleuropneumoniaeAdhesins, BacterialAnimalsBacterial Proteinsbcl-2-Associated X ProteinCaspase 9Cytokinesfas ReceptorFlow CytometryGene DeletionGene Expression ProfilingHEK293 CellsHumansInflammationInterleukin-8Adhesins, BacterialBacterial Proteinsbcl-2-Associated X ProteinCaspase 9Cytokinesfas ReceptorInterleukin-8p38 Mitogen-Activated Protein KinasesReceptors, G-Protein-CoupledReceptors, OdorantVirulence Factors

Identifiers

PMID27046446
PMCPMC4820727
OpenAlexW2317241558

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.