Evidence map›Paper›PMID 25847914›Full record

ArticlePhysiological reports2015

Comprehensive evaluation of poly(I:C) induced inflammatory response in an airway epithelial model.

Amanda R Lever, Hyoungshin Park, Thomas J Mulhern, George R Jackson, James C Comolli, Jeffrey T Borenstein, Patrick J Hayden, Rachelle Prantil-Baun

Open access · goldAbstract read
In one paragraph

Article in Physiological reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

35 citing papers in PubMed, 58 citations in OpenAlex.

  1. Trial
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  4. Protocol for differentiating primary human small airway epithelial cells at the air-liquid interface.American journal of physiology. Lung cellular and molecular physiology · 2025
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  14. Effects ofFoods (Basel, Switzerland) · 2023
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  18. Potentiation of long-acting βRespiratory research · 2021
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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 3 institutions in 1 country.

Amanda R LeverCharles Stark Draper Laboratory, Cambridge, Massachusetts.
Hyoungshin ParkCharles Stark Draper Laboratory, Cambridge, Massachusetts.
Thomas J MulhernCharles Stark Draper Laboratory, Cambridge, Massachusetts.
George R JacksonMatTek Corporation, Ashland, Massachusetts.
James C ComolliCharles Stark Draper Laboratory, Cambridge, Massachusetts.
Jeffrey T BorensteinCharles Stark Draper Laboratory, Cambridge, Massachusetts.
Patrick J HaydenMatTek Corporation, Ashland, Massachusetts.
Rachelle Prantil-BaunCharles Stark Draper Laboratory, Cambridge, Massachusetts rprantilbaun@draper.com.
Draper Laboratory · USAshland (United States) · USMatTek Corporation (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Respiratory viruses invade the upper airway of the lung, triggering a potent immune response that often exacerbates preexisting conditions such as asthma and COPD. Poly(I:C) is a synthetic analog of viral dsRNA that induces the characteristic inflammatory response associated with viral infection, such as loss of epithelial integrity, and increased production of mucus and inflammatory cytokines. Here, we explore the mechanistic responses to poly(I:C) in a well-defined primary normal human bronchial epithelial (NHBE) model that recapitulates in vivo functions and responses. We developed functional and quantifiable methods to evaluate the physiology of our model in both healthy and inflamed states. Through gene and protein expression, we validated the differentiation state and population of essential cell subtypes (i.e., ciliated, goblet, club, and basal cells) as compared to the human lung. Assays for total mucus production, cytokine secretion, and barrier function were used to evaluate in vitro physiology and response to viral insult. Cells were treated apically with poly(I:C) and evaluated 48 h after induction. Results revealed a dose-dependent increase in goblet cell differentiation, as well as, an increase in mucus production relative to controls. There was also a dose-dependent increase in secretion of IL-6, IL-8, TNF-α, and RANTES. Epithelial barrier function, as measured by TEER, was maintained at 1501 ± 355 Ω*cm² postdifferentiation, but dropped significantly when challenged with poly(I:C). This study provides first steps toward a well-characterized model with defined functional methods for understanding dsRNA stimulated inflammatory responses in a physiologically relevant manner.

Indexed as

Airway epithelial cellsinterleukin‐8mucuspoly(I:C)

Identifiers

PMID25847914
PMCPMC4425952
OpenAlexW2110628542

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.