Evidence map›Paper›PMID 27548479›Full record

ArticlePLoS pathogens2016

Evidence and Role for Bacterial Mucin Degradation in Cystic Fibrosis Airway Disease.

Jeffrey M Flynn, David Niccum, Jordan M Dunitz, Ryan C Hunter

Abstract read
In one paragraph

Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 142 papers.

0numbers the graph read from it
0cells of the map it votes in
142citing papers in PubMed
–field-weighted citation impact
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

142 citing papers in PubMed.

  1. Journal of bacteriology · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Functional CFTR may be required for Prevotella melaninogenica regulation of epithelial cell defense against Staphylococcus aureus.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2026
    Article
  11. Mucin stimulates the growth ofMicrobiology (Reading, England) · 2026
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Activation of theInfection and immunity · 2025
    Article
  17. Article
  18. mBio · 2025
    Article
  19. Article
  20. Hyperconcentrated mucus in small airways: a mechanistic model for the pathogenesis of paediatric bronchiectasis.European respiratory review : an official journal of the European Respiratory Society · 2025
    Review

82 more citing papers are in PubMed but not listed here.

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.

Jeffrey M FlynnDepartment of Microbiology & Immunology, University of Minnesota, Minneapolis, Minnesota, United States of America.
David NiccumDivision of Pulmonary, Allergy, Critical Care & Sleep Medicine, University of Minnesota, Minneapolis, Minnesota, United States of America.
Jordan M DunitzDivision of Pulmonary, Allergy, Critical Care & Sleep Medicine, University of Minnesota, Minneapolis, Minnesota, United States of America.
Ryan C HunterDepartment of Microbiology & Immunology, University of Minnesota, Minneapolis, Minnesota, United States of America.ORCID 0000-0003-3841-1676

Funding

University of Minnesota Clinical and Translational Science Institute (UMN CTSI)UL1TR000114 · NCATS · UNIVERSITY OF MINNESOTA · PI BLAZAR, BRUCE R · 2012 to 2015
$35.0M
TRAINING-PULMONARY CELL &MOLECULAR BIOLOGY &PHYSIOLOGYT32HL007741 · NHLBI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI DUDLEY, R. ADAMS, INGBAR, DAVID H · 1994 to 2023
$13.9M
Spatial characterization of microbial communities in the cystic fibrosis lungR00HL114862 · NHLBI · UNIVERSITY OF MINNESOTA · PI HUNTER, RYAN COULSON · 2013 to 2015
$713k
NCATS NIH HHS UL1 TR000114NHLBI NIH HHS R00 HL114862NHLBI NIH HHS T32 HL007741
6 · The paper itself

Abstract

Chronic lung infections in cystic fibrosis (CF) patients are composed of complex microbial communities that incite persistent inflammation and airway damage. Despite the high density of bacteria that colonize the lower airways, nutrient sources that sustain bacterial growth in vivo, and how those nutrients are derived, are not well characterized. In this study, we examined the possibility that mucins serve as an important carbon reservoir for the CF lung microbiota. While Pseudomonas aeruginosa was unable to efficiently utilize mucins in isolation, we found that anaerobic, mucin-fermenting bacteria could stimulate the robust growth of CF pathogens when provided intact mucins as a sole carbon source. 16S rRNA sequencing and enrichment culturing of sputum also identified that mucin-degrading anaerobes are ubiquitous in the airways of CF patients. The collective fermentative metabolism of these mucin-degrading communities in vitro generated amino acids and short chain fatty acids (propionate and acetate) during growth on mucin, and the same metabolites were also found in abundance within expectorated sputum. The significance of these findings was supported by in vivo P. aeruginosa gene expression, which revealed a heightened expression of genes required for the catabolism of propionate. Given that propionate is exclusively derived from bacterial fermentation, these data provide evidence for an important role of mucin fermenting bacteria in the carbon flux of the lower airways. More specifically, microorganisms typically defined as commensals may contribute to airway disease by degrading mucins, in turn providing nutrients for pathogens otherwise unable to efficiently obtain carbon in the lung.

Indexed as

Cystic FibrosisFemaleHumansLungMaleMucinsPropionatesPseudomonas aeruginosaRNA, BacterialRNA, Ribosomal, 16SMucinsPropionatesRNA, BacterialRNA, Ribosomal, 16S

Identifiers

PMID27548479
PMCPMC4993466

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.