Evidence map›Paper›PMID 26851259›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2016

Increased susceptibility of Cftr-/- mice to LPS-induced lung remodeling.

Emanuela M Bruscia, Ping-Xia Zhang, Christina Barone, Bob J Scholte, Robert Homer, Diane S Krause, Marie E Egan

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

25 citing papers in PubMed, 37 citations in OpenAlex.

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  9. Review
  10. To bead or not to bead: A review ofFrontiers in physiology · 2023
    Review
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  15. Article
  16. Fibrocyte accumulation in the lungs of cystic fibrosis patients.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2020
    Article
  17. Review
  18. AGTR2 absence or antagonism prevents cystic fibrosis pulmonary manifestations.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2019
    Article
  19. Review
  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

7 authors at 2 institutions in 2 countries.

Emanuela M BrusciaDepartment of Pediatrics, Yale University School of Medicine, New Haven, Connecticut;
Ping-Xia ZhangDepartment of Laboratory Medicine, Yale University School of Medicine, New Haven, Connecticut;
Christina BaroneDepartment of Pediatrics, Yale University School of Medicine, New Haven, Connecticut;
Bob J ScholteDepartment of Cell Biology, Erasmus Medical Centre, Rotterdam, The Netherlands.
Robert HomerDepartment of Pathology, Yale University School of Medicine, New Haven, Connecticut;
Diane S KrauseDepartment of Laboratory Medicine, Yale University School of Medicine, New Haven, Connecticut; Department of Pathology, Yale University School of Medicine, New Haven, Connecticut;
Marie E EganDepartment of Pediatrics, Yale University School of Medicine, New Haven, Connecticut; Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Connecticut; and marie.egan@yale.edu.
Yale University · USErasmus University Rotterdam · NL

Funding

Yale Cooperative Hematology Specialized Core CenterU54DK106857 · NIDDK · YALE UNIVERSITY · PI JOHN HWA, Diane S Krause · 2015 to 2026
$9.7M
CFTR and the Immune ResponseR01HL093004 · NHLBI · YALE UNIVERSITY · PI BRUSCIA, EMANUELA MARINA, EGAN, MARIE E · 2010 to 2014
$2.0M
NHLBI NIH HHS R01 HL093004NIDDK NIH HHS U54 DK106857
6 · The paper itself

Abstract

Cystic fibrosis (CF) is caused by homozygous mutations of the CF transmembrane conductance regulator (CFTR) Cl(-) channel, which result in chronic pulmonary infection and inflammation, the major cause of morbidity and mortality. Although these processes are clearly related to each other, each is likely to contribute to the pathology differently. Understanding the contribution of each of these processes to the overall pathology has been difficult, because they are usually so intimately connected. Various CF mouse models have demonstrated abnormal immune responses compared with wild-type (WT) littermates when challenged with live bacteria or bacterial products acutely. However, these studies have not investigated the consequences of persistent inflammation on lung tissue in CF mice, which may better model the lung pathology in patients. We characterized the lung pathology and immune response of Cftr(-/-) (CF) and Cftr(+/+) (WT) mice to chronic administration of Pseudomonas aeruginosa lipopolysaccharide (LPS). We show that, after long-term repeated LPS exposure, CF mice develop an abnormal and persistent immune response, which is associated with more robust structural changes in the lung than those observed in WT mice. Although CF mice and their WT littermates develop lung pathology after chronic exposure to LPS, the inflammation and damage resolve in WT mice. However, CF mice do not recover efficiently, and, as a consequence of their chronic inflammation, CF mice are more susceptible to morphological changes and lung remodeling. This study shows that chronic inflammation alone contributes significantly to aspects of CF lung pathology.

Indexed as

Airway RemodelingAnimalsChemokine CXCL10Cystic FibrosisCystic Fibrosis Transmembrane Conductance RegulatorLipopolysaccharidesLungMice, 129 StrainMice, Inbred C57BLMice, Inbred CFTRMice, KnockoutPneumoniaRespiratory MucosaChemokine CXCL10Cxcl10 protein, mouseCystic Fibrosis Transmembrane Conductance RegulatorLipopolysaccharidescystic fibrosisIFN-γ-induced protein 10inflammation

Identifiers

PMID26851259
PMCPMC4836110
OpenAlexW2330056636

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.