Evidence map›Paper›PMID 27169516›Full record

ArticleBMC genomics2016

Mapping genetic determinants of host susceptibility to Pseudomonas aeruginosa lung infection in mice.

Maura De Simone, Lorenza Spagnuolo, Nicola Ivan Lorè, Cristina Cigana, Ida De Fino, Karl W Broman, Fuad A Iraqi, Alessandra Bragonzi

Open access · goldAbstract read
In one paragraph

Article in BMC genomics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.7field-weighted citation impact, top 26% 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

11 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
  2. Article
  3. G9a promotes inflammation inAnnals of translational medicine · 2022
    Article
  4. Review
  5. Extract FromFrontiers in pharmacology · 2021
    Article
  6. Article
  7. Article
  8. Article
  9. The Collaborative Cross mouse model for dissecting genetic susceptibility to infectious diseases.Mammalian genome : official journal of the International Mammalian Genome Society · 2018
    Review
  10. The impact of host genetic background in the Pseudomonas aeruginosa respiratory infections.Mammalian genome : official journal of the International Mammalian Genome Society · 2018
    Review
  11. 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

8 authors at 4 institutions in 3 countries.

Maura De SimoneInfection and Cystic Fibrosis Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy.
Lorenza SpagnuoloInfection and Cystic Fibrosis Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy.
Nicola Ivan LorèInfection and Cystic Fibrosis Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy.
Cristina CiganaInfection and Cystic Fibrosis Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy.
Ida De FinoInfection and Cystic Fibrosis Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy.
Karl W BromanDepartment of Biostatistics & Medical Informatics, University of Wisconsin, Madison, WI, USA.
Fuad A IraqiDepartment of Clinical Microbiology and Immunology, Sackler Faculty of Medicine, Tel Aviv University, Ramat Aviv, 69978, Tel Aviv, Israel.
Alessandra BragonziInfection and Cystic Fibrosis Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. bragonzi.alessandra@hsr.it.
Istituto di Ricovero e Cura a Carattere Scientifico San RaffaeleTel Aviv University · ILUniversity of Wisconsin–Madison · USVita-Salute San Raffaele University · IT

Funding

Systems Genetic Analysis of Multi-parent CrossesR01GM070683 · NIGMS · JACKSON LABORATORY · PI BROMAN, KARL W, CHURCHILL, GARY A · 2004 to 2022
$6.8M
NIGMS NIH HHS R01 GM070683
6 · The paper itself

Abstract

backgroundP. aeruginosa is one of the top three causes of opportunistic human bacterial infections. The remarkable variability in the clinical outcomes of this infection is thought to be associated with genetic predisposition. However, the genes underlying host susceptibility to P. aeruginosa infection are still largely unknown.

resultsAs a step towards mapping these genes, we applied a genome wide linkage analysis approach to a mouse model. A large F2 intercross population, obtained by mating P. aeruginosa-resistant C3H/HeOuJ, and susceptible A/J mice, was used for quantitative trait locus (QTL) mapping. The F2 progenies were challenged with a P. aeruginosa clinical strain and monitored for the survival time up to 7 days post-infection, as a disease phenotype associated trait. Selected phenotypic extremes of the F2 distribution were genotyped with high-density single nucleotide polymorphic (SNP) markers, and subsequently QTL analysis was performed. A significant locus was mapped on chromosome 6 and was named P . aeruginosa infection resistance locus 1 (Pairl1). The most promising candidate genes, including Dok1, Tacr1, Cd207, Clec4f, Gp9, Gata2, Foxp1, are related to pathogen sensing, neutrophils and macrophages recruitment and inflammatory processes.

conclusionsWe propose a set of genes involved in the pathogenesis of P. aeruginosa infection that may be explored to complement human studies.

Indexed as

Gene Regulatory NetworksAnimalsChromosome MappingDisease Models, AnimalGenetic LinkageGenetic Predisposition to DiseaseHumansMicePolymorphism, Single NucleotidePseudomonas aeruginosaPseudomonas InfectionsQuantitative Trait LociCandidate genesHost susceptibilityLinkage analysisMurine modelP. aeruginosaPneumoniaQTL mapping

Identifiers

PMID27169516
PMCPMC4866434
OpenAlexW2350596157

What OpenQuestion holds

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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.