Evidence map›Paper›PMID 23087427›Full record

ArticleThe Journal of infectious diseases2013

Response of CFTR-deficient mice to long-term chronic Pseudomonas aeruginosa infection and PTX3 therapy.

Moira Paroni, Federica Moalli, Manuela Nebuloni, Fabio Pasqualini, Tracey Bonfield, Alessandro Nonis, Alberto Mantovani, Cecilia Garlanda, Alessandra Bragonzi

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of infectious diseases, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

32 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
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  5. Review
  6. Article
  7. International journal of molecular sciences · 2021
    Article
  8. Article
  9. Review
  10. Article
  11. The Long Pentraxin PTX3 ControlsFrontiers in immunology · 2021
    Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Pentraxin 3 deletion aggravates allergic inflammation through a TThe Journal of allergy and clinical immunology · 2017
    Article
  18. Article
  19. Increased susceptibility of Cftr-/- mice to LPS-induced lung remodeling.American journal of physiology. Lung cellular and molecular physiology · 2016
    Article
  20. 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

9 authors at 4 institutions in 2 countries.

Moira ParoniInfection and Cystic Fibrosis Unit, Division of Immunology, Transplantation, and Infectious Diseases, San Raffaele Scientific Institute, Via Olgettina 58, Milan, Italy.
Federica Moalli
Manuela Nebuloni
Fabio Pasqualini
Tracey Bonfield
Alessandro Nonis
Alberto Mantovani
Cecilia Garlanda
Alessandra Bragonzi
Humanitas University · ITVita-Salute San Raffaele University · ITUniversity of Milan · ITCase Western Reserve University · US

Funding

Translational Research in Cystic FibrosisP30DK027651 · NIDDK · CASE WESTERN RESERVE UNIVERSITY · PI DRUMM, MITCHELL L · 1986 to 2014
$15.6M
NIDDK NIH HHS P30 DK027651Telethon GGP05095
6 · The paper itself

Abstract

backgroundIn cystic fibrosis (CF) patients, chronic lung infection and inflammation due to Pseudomonas aeruginosa contribute to the decline of lung function. The increased prevalence of multidrug resistance among bacteria and the adverse effects of antiinflammatory agents highlight the need for alternative therapeutic approaches that should be tested in a relevant animal model.

methodsGut-corrected CF and non-CF mice were chronically infected with a multidrug-resistant P. aeruginosa strain and treated with the long pentraxin PTX3. Body weight, bacterial count, inflammation, and lung pathology were evaluated after 12 days. PTX3 localization in CF sputum specimens was analyzed by immunofluorescence.

resultsChronic P. aeruginosa infection developed similarly in CF and non-CF mice but differed in terms of the inflammatory response. Leukocyte recruitment in the airways, cytokine levels, and chemokine levels were significantly higher in CF mice, compared with non-CF mice. PTX3 treatment, which facilitates phagocytosis of pathogens, reduced P. aeruginosa colonization and restored airway inflammation in CF mice to levels observed in non-CF mice. The presence of PTX3 in CF sputum, in leukocytes, or bound to P. aeruginosa macrocolonies, as well as previous data on PTX3 polymorphisms in colonized CF patients, confirm the relevance of this molecule.

conclusionsThese findings represent a step forward in demonstrating the therapeutic potential of PTX3 in CF.

Indexed as

AnimalsC-Reactive ProteinFemaleFluorescent Antibody Technique, IndirectLungMaleMiceMice, Inbred CFTRPentraxinsPhagocytosisPseudomonas InfectionsRecombinant ProteinsSerum Amyloid P-ComponentC-Reactive ProteinPentraxinsRecombinant ProteinsSerum Amyloid P-ComponentCystic FibrosisinflammationMouse ModelPseudomonas InfectionPTX3Respiratory Tract Infections

Identifiers

PMID23087427
PMCPMC4055833
OpenAlexW2156842583

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.