Evidence map›Paper›PMID 30971247›Full record

ArticleRespiratory research2019

Salicylic acid amplifies Carbachol-induced bronchoconstriction in human precision-cut lung slices.

Joseph Jude, Danielle Botelho, Nikhil Karmacharya, Gao Yuan Cao, William Jester, Reynold A Panettieri

Open access · goldAbstract read
In one paragraph

Article in Respiratory research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

12 citing papers in PubMed, 24 citations in OpenAlex.

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  12. Evaluation of bronchodialatory and antimicrobial activities ofSaudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2020
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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

6 authors at 2 institutions in 1 country.

Joseph JudeRutgers Institute for Translational Medicine and Science (RITMS), Rutgers, The State University of New Jersey, Rm# 4276, 89 French Street, New Brunswick, NJ08901, USA. joseph.antonyjude@rutgers.edu.
Danielle BotelhoResearch Institute for Fragrance Materials (RIFM), Woodcliff Lake, New Jersey, USA.
Nikhil KarmacharyaRutgers Institute for Translational Medicine and Science (RITMS), Rutgers, The State University of New Jersey, Rm# 4276, 89 French Street, New Brunswick, NJ08901, USA.
Gao Yuan CaoRutgers Institute for Translational Medicine and Science (RITMS), Rutgers, The State University of New Jersey, Rm# 4276, 89 French Street, New Brunswick, NJ08901, USA.
William JesterRutgers Institute for Translational Medicine and Science (RITMS), Rutgers, The State University of New Jersey, Rm# 4276, 89 French Street, New Brunswick, NJ08901, USA.
Reynold A PanettieriRutgers Institute for Translational Medicine and Science (RITMS), Rutgers, The State University of New Jersey, Rm# 4276, 89 French Street, New Brunswick, NJ08901, USA.
Rutgers, The State University of New Jersey · USResearch Institute for Fragrance Materials · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAsthma exacerbations evoke emergency room visits, progressive loss of lung function and increased mortality. Environmental and industrial toxicants exacerbate asthma, although the underlying mechanisms are unknown. We assessed whether 3 distinct toxicants, salicylic acid (SA), toluene diisocyanate (TDI), and 1-chloro-2,4-dinitrobenzene (DNCB) induced airway hyperresponsiveness (AHR) through modulating excitation-contraction coupling in human airway smooth muscle (HASM) cells. The toxicants include a non-sensitizing irritant (SA), respiratory sensitizer (TDI) and dermal sensitizer (DNCB), respectively. We hypothesized that these toxicants induce AHR by modulating excitation-contraction (EC) coupling in airway smooth muscle (ASM) cells.

methodsCarbachol-induced bronchoconstriction was measured in precision-cut human lung slices (hPCLS) following exposure to SA, TDI, DNCB or vehicle. Culture supernatants of hPCLS were screened for mediator release. In HASM cells treated with the toxicants, surrogate readouts of EC coupling were measured by phosphorylated myosin light chain (pMLC) and agonist-induced Ca

resultsIn hPCLS, SA, but not TDI or DNCB, potentiated carbachol-induced bronchoconstriction. The toxicants had little effect on release of inflammatory mediators, including IL-6, IL-8 and eotaxin from hPCLS. In HASM cells, TDI amplified carbachol-induced MLC phosphorylation. The toxicants also had little effect on agonist-induced [Ca IMPLICATIONS: Our findings suggest that non-sensitizing irritant salicylic acid may evoke AHR and exacerbate symptoms in susceptible individuals or in those with underlying lung disease.

Indexed as

BronchoconstrictionCarbacholCells, CulturedDose-Response Relationship, DrugDrug SynergismHumansIrritantsLungSalicylic AcidCarbacholIrritantsSalicylic Acid

Identifiers

PMID30971247
PMCPMC6458705
OpenAlexW2945087045

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.