Evidence map›Paper›PMID 26483403›Full record

ArticleInfection and immunity2016

Surface Polysaccharide Mutants Reveal that Absence of O Antigen Reduces Biofilm Formation of Actinobacillus pleuropneumoniae.

S Hathroubi, M A Hancock, J T Bossé, P R Langford, Y D N Tremblay, J Labrie, M Jacques

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 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

26 citing papers in PubMed, 41 citations in OpenAlex.

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  16. Quinolone Resistance ofInternational journal of molecular sciences · 2021
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  20. Helicobacter pylori Biofilm Formation and Its Potential Role in Pathogenesis.Microbiology and molecular biology reviews : MMBR · 2018
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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 at 3 institutions in 2 countries.

S HathroubiGroupe de Recherche sur les Maladies Infectieuses du Porc, Faculté de Médecine Vétérinaire, Université de Montréal, St-Hyacinthe, Québec, Canada.
M A HancockMcGill Surface Plasmon Resonance-Mass Spectrometry Facility, McGill University, Montréal, Québec, Canada.
J T BosséSection of Paediatrics, Imperial College London, London, United Kingdom.ORCID http://orcid.org/0000-0002-8491-4779
P R LangfordSection of Paediatrics, Imperial College London, London, United Kingdom.
Y D N TremblayGroupe de Recherche sur les Maladies Infectieuses du Porc, Faculté de Médecine Vétérinaire, Université de Montréal, St-Hyacinthe, Québec, Canada.
J LabrieGroupe de Recherche sur les Maladies Infectieuses du Porc, Faculté de Médecine Vétérinaire, Université de Montréal, St-Hyacinthe, Québec, Canada.
M JacquesGroupe de Recherche sur les Maladies Infectieuses du Porc, Faculté de Médecine Vétérinaire, Université de Montréal, St-Hyacinthe, Québec, Canada mario.jacques@umontreal.ca.
Université de Montréal · CAImperial College London · GBMcGill University · CA

Funding

Biotechnology and Biological Sciences Research Council BB/G018553/1
6 · The paper itself

Abstract

Actinobacillus pleuropneumoniae is a Gram-negative bacterium belonging to the Pasteurellaceae family and the causative agent of porcine pleuropneumonia, a highly contagious lung disease causing important economic losses. Surface polysaccharides, including lipopolysaccharides (LPS) and capsular polysaccharides (CPS), are implicated in the adhesion and virulence of A. pleuropneumoniae, but their role in biofilm formation is still unclear. In this study, we investigated the requirement for these surface polysaccharides in biofilm formation by A. pleuropneumoniae serotype 1. Well-characterized mutants were used: an O-antigen LPS mutant, a truncated core LPS mutant with an intact O antigen, a capsule mutant, and a poly-N-acetylglucosamine (PGA) mutant. We compared the amount of biofilm produced by the parental strain and the isogenic mutants using static and dynamic systems. Compared to the findings for the biofilm of the parental or other strains, the biofilm of the O antigen and the PGA mutants was dramatically reduced, and it had less cell-associated PGA. Real-time PCR analyses revealed a significant reduction in the level of pgaA, cpxR, and cpxA mRNA in the biofilm cells of the O-antigen mutant compared to that in the biofilm cells of the parental strain. Specific binding between PGA and LPS was consistently detected by surface plasmon resonance, but the lack of O antigen did not abolish these interactions. In conclusion, the absence of the O antigen reduces the ability of A. pleuropneumoniae to form a biofilm, and this is associated with the reduced expression and production of PGA.

Indexed as

Actinobacillus InfectionsActinobacillus pleuropneumoniaeAnimalsBacterial AdhesionBacterial CapsulesBacterial Outer Membrane ProteinsBacterial ProteinsBiofilmsLipopolysaccharidesO AntigensProtein BindingProtein KinasesSwineSwine DiseasesBacterial Outer Membrane ProteinsBacterial ProteinsCpxA protein, bacteriaCpxR protein, BacteriaLipopolysaccharidesO AntigensProtein Kinases

Identifiers

PMID26483403
PMCPMC4694004
OpenAlexW2263441127

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.