Evidence map›Paper›PMID 32985670›Full record

ArticleBioscience reports2020

Epithelial barrier function properties of the 16HBE14o- human bronchial epithelial cell culture model.

Patrick J Callaghan, Bryan Ferrick, Elizabeth Rybakovsky, Sunil Thomas, James M Mullin

Open access · goldAbstract read
In one paragraph

Article in Bioscience reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 6% 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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

  1. Programmed cell death in human respiratory syncytial virus infection.Frontiers in cellular and infection microbiology · 2025
    Pooled it
  2. In vitro approaches to assess respiratory toxicity from volatile organic compounds: an in-depth review.Toxicological sciences : an official journal of the Society of Toxicology · 2026
    Review
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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

5 authors at 2 institutions in 1 country.

Patrick J CallaghanLankenau Institute for Medical Research, 100 Lancaster Avenue, Wynnewood, PA 19096, U.S.A.
Bryan FerrickDepartment of Biomedical Engineering, Drexel University, Philadelphia, PA 19104, U.S.A.
Elizabeth RybakovskyLankenau Institute for Medical Research, 100 Lancaster Avenue, Wynnewood, PA 19096, U.S.A.
Sunil ThomasLankenau Institute for Medical Research, 100 Lancaster Avenue, Wynnewood, PA 19096, U.S.A.
James M MullinLankenau Institute for Medical Research, 100 Lancaster Avenue, Wynnewood, PA 19096, U.S.A.
Lankenau Institute for Medical Research · USDrexel University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The human bronchial epithelial cell line, 16HBE14o- (16HBE), is widely used as a model for respiratory epithelial diseases and barrier function. During differentiation, transepithelial electrical resistance (TER) increased to approximately 800 Ohms × cm2, while 14C-d-mannitol flux rates (Jm) simultaneously decreased. Tight junctions (TJs) were shown by diffusion potential studies to be anion-selective with PC1/PNa = 1.9. Transepithelial leakiness could be induced by the phorbol ester, protein kinase C (PKC) activator, 12-O-tetradecanoylphorbol-13-acetate (TPA), and the proinflammatory cytokine, tumor necrosis factor-α (TNF-α). Basal barrier function could not be improved by the micronutrients, zinc, or quercetin. Of methodological significance, TER was observed to be more variable and to spontaneously, significantly decrease after initial barrier formation, whereas Jm did not significantly fluctuate or increase. Unlike the strong inverse relationship between TER and Jm during differentiation, differentiated cell layers manifested no relationship between TER and Jm. There was also much greater variability for TER values compared with Jm. Investigating the dependence of 16HBE TER on transcellular ion conductance, inhibition of the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) chloride channel with GlyH-101 produced a large decrease in short-circuit current (Isc) and a slight increase in TER, but no significant change in Jm. A strong temperature dependence was observed not only for Isc, but also for TER. In summary, research utilizing 16HBE as a model in airway barrier function studies needs to be aware of the complexity of TER as a parameter of barrier function given the influence of CFTR-dependent transcellular conductance on TER.

Indexed as

BronchiCell Culture TechniquesCell DifferentiationCell LineCell Membrane PermeabilityCystic Fibrosis Transmembrane Conductance RegulatorElectric ImpedanceEpithelial CellsGlycineHumansHydrazinesMannitolRespiratory MucosaRespiratory Tract DiseasesTight JunctionsCFTR protein, humanCystic Fibrosis Transmembrane Conductance RegulatorGlycineHydrazinesMannitolN-(2-naphthalenyl)-((3,5-dibromo-2,4-dihydroxyphenyl)methylene)glycine hydrazidebarrier functionbronchialCFTRtight junctiontransepithelial electrical resistancetumour necrosis factors

Identifiers

PMID32985670
PMCPMC7569203
OpenAlexW3089220385

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.