Evidence map›Paper›PMID 24917822›Full record

ArticleFrontiers in physiology2014

The buffer capacity of airway epithelial secretions.

Dusik Kim, Jie Liao, John W Hanrahan

Open access · goldAbstract read
In one paragraph

Article in Frontiers in physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.9field-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

20 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Targeting ATP12A, a Nongastric Proton Pump α Subunit, for Idiopathic Pulmonary Fibrosis Treatment.American journal of respiratory cell and molecular biology · 2023
    Article
  3. Review
  4. Article
  5. Heme Peroxidases at Unperturbed and Inflamed Mucous Surfaces.Antioxidants (Basel, Switzerland) · 2021
    Review
  6. Article
  7. Is CFTR an exchanger?: Regulation of HCOBiochemistry and biophysics reports · 2021
    Article
  8. Article
  9. Article
  10. Environmental and Endogenous Acids Can Trigger Allergic-Type Airway Reactions.International journal of environmental research and public health · 2020
    Review
  11. Article
  12. Article
  13. Article
  14. Tracheal acid or surfactant instillation raises alveolar surface tension.Journal of applied physiology (Bethesda, Md. : 1985) · 2018
    Article
  15. Article
  16. Article
  17. Relationships among CFTR expression, HCO3- secretion, and host defense may inform gene- and cell-based cystic fibrosis therapies.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  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

3 authors at 1 institution in 1 country.

Dusik KimDepartment of Physiology, McGill University Montréal, QC, Canada.
Jie LiaoDepartment of Physiology, McGill University Montréal, QC, Canada.
John W HanrahanDepartment of Physiology, McGill University Montréal, QC, Canada ; McGill University Health Centre Research Institute Montréal, QC, Canada.
McGill University · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The pH of airway epithelial secretions influences bacterial killing and mucus properties and is reduced by acidic pollutants, gastric reflux, and respiratory diseases such as cystic fibrosis (CF). The effect of acute acid loads depends on buffer capacity, however the buffering of airway secretions has not been well characterized. In this work we develop a method for titrating micro-scale (30 μl) volumes and use it to study fluid secreted by the human airway epithelial cell line Calu-3, a widely used model for submucosal gland serous cells. Microtitration curves revealed that HCO(-) 3 is the major buffer. Peak buffer capacity (β) increased from 17 to 28 mM/pH during forskolin stimulation, and was reduced by >50% in fluid secreted by cystic fibrosis transmembrane conductance regulator (CFTR)-deficient Calu-3 monolayers, confirming an important role of CFTR in HCO(-) 3 secretion. Back-titration with NaOH revealed non-volatile buffer capacity due to proteins synthesized and released by the epithelial cells. Lysozyme and mucin concentrations were too low to buffer Calu-3 fluid significantly, however model titrations of porcine gastric mucins at concentrations near the sol-gel transition suggest that mucins may contribute to the buffer capacity of ASL in vivo. We conclude that CFTR-dependent HCO(-) 3 secretion and epithelially-derived proteins are the predominant buffers in Calu-3 secretions.

Indexed as

airway submucosal glandsbicarbonate secretionCFTRcystic fibrosis

Identifiers

PMID24917822
PMCPMC4042063
OpenAlexW2078894138

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.