Evidence map›Paper›PMID 25816137›Full record

ArticlePloS one2015

Pulmonary inflammation is regulated by the levels of the vesicular acetylcholine transporter.

Nathalia M Pinheiro, Claudia J C P Miranda, Adenir Perini, Niels O S Câmara, Soraia K P Costa, Maria Isabel C Alonso-Vale, Luciana C Caperuto, Iolanda F L C Tibério, Marco Antônio M Prado, Mílton A Martins and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
4.1field-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

22 citing papers in PubMed, 54 citations in OpenAlex.

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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

12 authors at 3 institutions in 2 countries.

Nathalia M PinheiroDepartment of Medicine, School of Medicine, University of Sao Paulo, São Paulo, Brazil.
Claudia J C P MirandaDepartment of Medicine, School of Medicine, University of Sao Paulo, São Paulo, Brazil.
Adenir PeriniDepartment of Medicine, School of Medicine, University of Sao Paulo, São Paulo, Brazil.
Niels O S CâmaraDepartment of Immunology, Institute of Biomedical Sciences, University of Sao Paulo, São Paulo, Brazil.
Soraia K P CostaDepartment of Pharmacology Institute of Biomedical Sciences, University of Sao Paulo, São Paulo, Brazil.
Maria Isabel C Alonso-ValeDepartment of Biological Science, Federal University of Sao Paulo, Diadema, Brazil.
Luciana C CaperutoDepartment of Biological Science, Federal University of Sao Paulo, Diadema, Brazil.
Iolanda F L C TibérioDepartment of Medicine, School of Medicine, University of Sao Paulo, São Paulo, Brazil.
Marco Antônio M PradoMolecular Medicine Group, Robarts Research Institute, Department of Physiology & Pharmacology and Department of Anatomy & Cell Biology, University of Western Ontario, London, Canada.
Mílton A MartinsDepartment of Medicine, School of Medicine, University of Sao Paulo, São Paulo, Brazil.
Vânia F PradoMolecular Medicine Group, Robarts Research Institute, Department of Physiology & Pharmacology and Department of Anatomy & Cell Biology, University of Western Ontario, London, Canada.
Carla M PradoDepartment of Medicine, School of Medicine, University of Sao Paulo, São Paulo, Brazil; Department of Biological Science, Federal University of Sao Paulo, Diadema, Brazil.
Universidade de São Paulo · BRUniversidade Federal de São Paulo · BRWestern University · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acetylcholine (ACh) plays a crucial role in physiological responses of both the central and the peripheral nervous system. Moreover, ACh was described as an anti-inflammatory mediator involved in the suppression of exacerbated innate response and cytokine release in various organs. However, the specific contributions of endogenous release ACh for inflammatory responses in the lung are not well understood. To address this question we have used mice with reduced levels of the vesicular acetylcholine transporter (VAChT), a protein required for ACh storage in secretory vesicles. VAChT deficiency induced airway inflammation with enhanced TNF-α and IL-4 content, but not IL-6, IL-13 and IL-10 quantified by ELISA. Mice with decreased levels of VAChT presented increased collagen and elastic fibers deposition in airway walls which was consistent with an increase in inflammatory cells positive to MMP-9 and TIMP-1 in the lung. In vivo lung function evaluation showed airway hyperresponsiveness to methacholine in mutant mice. The expression of nuclear factor-kappa B (p65-NF-kB) in lung of VAChT-deficient mice were higher than in wild-type mice, whereas a decreased expression of janus-kinase 2 (JAK2) was observed in the lung of mutant animals. Our findings show the first evidence that cholinergic deficiency impaired lung function and produce local inflammation. Our data supports the notion that cholinergic system modulates airway inflammation by modulation of JAK2 and NF-kB pathway. We proposed that intact cholinergic pathway is necessary to maintain the lung homeostasis.

Indexed as

AcetylcholineAnimalsBlotting, WesternCells, CulturedCytokinesEdemaImmunoenzyme TechniquesLungMaleMiceMice, KnockoutNF-kappa BPneumoniaReal-Time Polymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionRNA, MessengerAcetylcholineCytokinesNF-kappa BRNA, MessengerSlc18a3 protein, mouseVesicular Acetylcholine Transport Proteins

Identifiers

PMID25816137
PMCPMC4376856
OpenAlexW2018904543

What OpenQuestion holds

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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.