Evidence map›Paper›PMID 26586376›Full record

ArticleDrug metabolism and disposition: the biological fate of chemicals2016

Glucocorticoid Clearance and Metabolite Profiling in an In Vitro Human Airway Epithelium Lung Model.

Dinelia Rivera-Burgos, Ujjal Sarkar, Amanda R Lever, Michael J Avram, Jonathan R Coppeta, John S Wishnok, Jeffrey T Borenstein, Steven R Tannenbaum

Open access · bronzeAbstract read
In one paragraph

Article in Drug metabolism and disposition: the biological fate of chemicals, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.5field-weighted citation impact, top 33% 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

5 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
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  3. 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

8 authors at 2 institutions in 1 country.

Dinelia Rivera-BurgosDepartment of Biological Engineering (D.R.B., U.S., J.S.W., S.R.T.), and Department of Chemistry (S.R.T.), Massachusetts Institute of Technology, and The Charles Stark Draper Laboratory (A.R.L., J.R.C., J.T.B.), Cambridge, Massachusetts; and Northwestern University, Feinberg School of Medicine, Chicago, Illinois (M.J.A.).
Ujjal SarkarDepartment of Biological Engineering (D.R.B., U.S., J.S.W., S.R.T.), and Department of Chemistry (S.R.T.), Massachusetts Institute of Technology, and The Charles Stark Draper Laboratory (A.R.L., J.R.C., J.T.B.), Cambridge, Massachusetts; and Northwestern University, Feinberg School of Medicine, Chicago, Illinois (M.J.A.).
Amanda R LeverDepartment of Biological Engineering (D.R.B., U.S., J.S.W., S.R.T.), and Department of Chemistry (S.R.T.), Massachusetts Institute of Technology, and The Charles Stark Draper Laboratory (A.R.L., J.R.C., J.T.B.), Cambridge, Massachusetts; and Northwestern University, Feinberg School of Medicine, Chicago, Illinois (M.J.A.).
Michael J AvramDepartment of Biological Engineering (D.R.B., U.S., J.S.W., S.R.T.), and Department of Chemistry (S.R.T.), Massachusetts Institute of Technology, and The Charles Stark Draper Laboratory (A.R.L., J.R.C., J.T.B.), Cambridge, Massachusetts; and Northwestern University, Feinberg School of Medicine, Chicago, Illinois (M.J.A.).
Jonathan R CoppetaDepartment of Biological Engineering (D.R.B., U.S., J.S.W., S.R.T.), and Department of Chemistry (S.R.T.), Massachusetts Institute of Technology, and The Charles Stark Draper Laboratory (A.R.L., J.R.C., J.T.B.), Cambridge, Massachusetts; and Northwestern University, Feinberg School of Medicine, Chicago, Illinois (M.J.A.).
John S WishnokDepartment of Biological Engineering (D.R.B., U.S., J.S.W., S.R.T.), and Department of Chemistry (S.R.T.), Massachusetts Institute of Technology, and The Charles Stark Draper Laboratory (A.R.L., J.R.C., J.T.B.), Cambridge, Massachusetts; and Northwestern University, Feinberg School of Medicine, Chicago, Illinois (M.J.A.).
Jeffrey T BorensteinDepartment of Biological Engineering (D.R.B., U.S., J.S.W., S.R.T.), and Department of Chemistry (S.R.T.), Massachusetts Institute of Technology, and The Charles Stark Draper Laboratory (A.R.L., J.R.C., J.T.B.), Cambridge, Massachusetts; and Northwestern University, Feinberg School of Medicine, Chicago, Illinois (M.J.A.).
Steven R TannenbaumDepartment of Biological Engineering (D.R.B., U.S., J.S.W., S.R.T.), and Department of Chemistry (S.R.T.), Massachusetts Institute of Technology, and The Charles Stark Draper Laboratory (A.R.L., J.R.C., J.T.B.), Cambridge, Massachusetts; and Northwestern University, Feinberg School of Medicine, Chicago, Illinois (M.J.A.) srt@mit.edu.
Northwestern University · USDraper Laboratory · US

Funding

TOXICOLOGY CORE UNITP30ES002109 · NIEHS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI LEVINE, STUART S · 1985 to 2020
$25.6M
TRAINING GRANTS IN ENVIROMENTAL TOXICOLOGYT32ES007020 · NIEHS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI ESSIGMANN, JOHN M · 1985 to 2024
$13.1M
All-Human Microphysical Model of Metastasis TherapyUH2TR000496 · NCATS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI GRIFFITH, LINDA G · 2012 to 2013
$2.3M
NCATS NIH HHS 5-UH2-TR000496NCATS NIH HHS UH2 TR000496NIEHS NIH HHS P30 ES002109NIEHS NIH HHS P30-ES002109NIEHS NIH HHS T32 ES007020
6 · The paper itself

Abstract

The emergence of microphysiologic epithelial lung models using human cells in a physiologically relevant microenvironment has the potential to be a powerful tool for preclinical drug development and to improve predictive power regarding in vivo drug clearance. In this study, an in vitro model of the airway comprising human primary lung epithelial cells cultured in a microfluidic platform was used to establish a physiologic state and to observe metabolic changes as a function of glucocorticoid exposure. Evaluation of mucus production rate and barrier function, along with lung-specific markers, demonstrated that the lungs maintained a differentiated phenotype. Initial concentrations of 100 nM hydrocortisone (HC) and 30 nM cortisone (C) were used to evaluate drug clearance and metabolite production. Measurements made using ultra-high-performance liquid chromatography and high-mass-accuracy mass spectrometry indicated that HC metabolism resulted in the production of C and dihydrocortisone (diHC). When the airway model was exposed to C, diHC was identified; however, no conversion to HC was observed. Multicompartmental modeling was used to characterize the lung bioreactor data, and pharmacokinetic parameters, including elimination clearance and elimination half-life, were estimated. Polymerse chain reaction data confirmed overexpression of 11-β hydroxysteroid dehydrogenase 2 (11βHSD2) over 11βHSD1, which is biologically relevant to human lung. Faster metabolism was observed relative to a static model on elevated rates of C and diHC formation. Overall, our results demonstrate that this lung airway model has been successfully developed and could interact with other human tissues in vitro to better predict in vivo drug behavior.

Indexed as

Cells, CulturedCortisoneEpithelial CellsGlucocorticoidsHalf-LifeHumansHydrocortisoneLungRespiratory MucosaCortisoneGlucocorticoidsHydrocortisone

Identifiers

PMID26586376
PMCPMC4727117
OpenAlexW2172755367

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.