Evidence map›Paper›PMID 23527286›Full record

ArticlePloS one2013

Mucociliary clearance defects in a murine in vitro model of pneumococcal airway infection.

Manfred Fliegauf, Andreas F-P Sonnen, Bernhard Kremer, Philipp Henneke

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. 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
2.0field-weighted citation impact, top 14% 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, 39 citations in OpenAlex.

  1. Article
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  9. First contact: the role of respiratory cilia in host-pathogen interactions in the airways.American journal of physiology. Lung cellular and molecular physiology · 2020
    Review
  10. Article
  11. Bacterial aetiology of chronic otitis media with effusion in children - risk factors.Journal of otolaryngology - head & neck surgery = Le Journal d'oto-rhino-laryngologie et de chirurgie cervico-faciale · 2020
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Protein localization screeningJournal of cell science · 2018
    Article
  17. Frontiers in immunology · 2018
    Review
  18. Article
  19. 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

4 authors at 2 institutions in 1 country.

Manfred FliegaufCentre of Chronic Immunodeficiency, University Medical Centre Freiburg and University of Freiburg, Freiburg, Germany. manfred.fliegauf@uniklinik-freiburg.de
Andreas F-P Sonnen
Bernhard Kremer
Philipp Henneke
University Medical Center Freiburg · DEUniversity of Freiburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mucociliary airway clearance is an innate defense mechanism that protects the lung from harmful effects of inhaled pathogens. In order to escape mechanical clearance, airway pathogens including Streptococcus pneumoniae (pneumococcus) are thought to inactivate mucociliary clearance by mechanisms such as slowing of ciliary beating and lytic damage of epithelial cells. Pore-forming toxins like pneumolysin, may be instrumental in these processes. In a murine in vitro airway infection model using tracheal epithelial cells grown in air-liquid interface cultures, we investigated the functional consequences on the ciliated respiratory epithelium when the first contact with pneumococci is established. High-speed video microscopy and live-cell imaging showed that the apical infection with both wildtype and pneumolysin-deficient pneumococci caused insufficient fluid flow along the epithelial surface and loss of efficient clearance, whereas ciliary beat frequency remained within the normal range. Three-dimensional confocal microscopy demonstrated that pneumococci caused specific morphologic aberrations of two key elements in the F-actin cytoskeleton: the junctional F-actin at the apical cortex of the lateral cell borders and the apical F-actin, localized within the planes of the apical cell sides at the ciliary bases. The lesions affected the columnar shape of the polarized respiratory epithelial cells. In addition, the planar architecture of the entire ciliated respiratory epithelium was irregularly distorted. Our observations indicate that the mechanical supports essential for both effective cilia strokes and stability of the epithelial barrier were weakened. We provide a new model, where--in pneumococcal infection--persistent ciliary beating generates turbulent fluid flow at non-planar distorted epithelial surface areas, which enables pneumococci to resist mechanical cilia-mediated clearance.

Indexed as

ActinsAnimalsBacterial ProteinsCell Culture TechniquesCiliaEpithelial CellsFluorescent Antibody TechniqueImmunity, InnateMiceMicroscopy, ConfocalMicroscopy, VideoMucociliary ClearancePneumococcal InfectionsRespiratory Tract InfectionsStreptococcus pneumoniaeStreptolysinsActinsBacterial ProteinsplY protein, Streptococcus pneumoniaeStreptolysins

Identifiers

PMID23527286
PMCPMC3602288
OpenAlexW2003084689

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.