Evidence map›Paper›PMID 38961398›Full record

ArticleJournal of inflammation (London, England)2024

Effect of VAChT reduction on lung alterations induced by exposure to iron particles in an asthma model.

Tabata Maruyama Dos Santos, Renato Fraga Righetti, Leandro do Nascimento Camargo, Edna Aparecida Leick, Silvia Fukuzaki, Elaine Cristina de Campos, Thiago Tafarel Galli, Beatriz Mangueira Saraiva-Romanholo, Luana Laura Sales da Silva, Jéssica Anastácia Silva Barbosa and 13 more

Erratum issuedAbstract read
In one paragraph

Article in Journal of inflammation (London, England), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

23 authors.

Tabata Maruyama Dos SantosFaculdade de Medicina FMUSP, Universidade de Sao Paulo, São Paulo, SP, Brazil. tabatamaruyama@gmail.com.
Renato Fraga RighettiFaculdade de Medicina FMUSP, Universidade de Sao Paulo, São Paulo, SP, Brazil.
Leandro do Nascimento CamargoFaculdade de Medicina FMUSP, Universidade de Sao Paulo, São Paulo, SP, Brazil.
Edna Aparecida LeickFaculdade de Medicina FMUSP, Universidade de Sao Paulo, São Paulo, SP, Brazil.
Silvia FukuzakiFaculdade de Medicina FMUSP, Universidade de Sao Paulo, São Paulo, SP, Brazil.
Elaine Cristina de CamposFaculdade de Medicina FMUSP, Universidade de Sao Paulo, São Paulo, SP, Brazil.
Thiago Tafarel GalliFaculdade de Medicina FMUSP, Universidade de Sao Paulo, São Paulo, SP, Brazil.
Beatriz Mangueira Saraiva-RomanholoFaculdade de Medicina FMUSP, Universidade de Sao Paulo, São Paulo, SP, Brazil.
Luana Laura Sales da SilvaFaculdade de Medicina FMUSP, Universidade de Sao Paulo, São Paulo, SP, Brazil.
Jéssica Anastácia Silva BarbosaFaculdade de Medicina FMUSP, Universidade de Sao Paulo, São Paulo, SP, Brazil.
Juliana Morelli Lopes Gonçalves JoãoFaculdade de Medicina FMUSP, Universidade de Sao Paulo, São Paulo, SP, Brazil.
Carla Máximo PradoDepartment of Biosciences, Universidade Federal de São Paulo, Santos, Brazil.
Bianca Goulart de RezendeFaculdade de Medicina FMUSP, Universidade de Sao Paulo, São Paulo, SP, Brazil.
Christine Laure Marie BourotteInstituto de Geociências, Universidade de São Paulo, São Paulo, Brasil.
Fernanda Degobbi Tenorio Quirino Dos Santos LopesFaculdade de Medicina FMUSP, Universidade de Sao Paulo, São Paulo, SP, Brazil.
Milton de Arruda MartinsFaculdade de Medicina FMUSP, Universidade de Sao Paulo, São Paulo, SP, Brazil.
Isabela M BensenorFaculdade de Medicina FMUSP, Universidade de Sao Paulo, São Paulo, SP, Brazil.
João Vitor de Oliveira CirilloUniversity City of São Paulo (UNICID), São Paulo, Brazil.
Suellen Karoline Moreira BezerraFaculdade de Medicina FMUSP, Universidade de Sao Paulo, São Paulo, SP, Brazil.
Fabio José Alencar SilvaEscola Superior de Ciências da Santa Casa de Misericórdia de Vitória, Vitória, Brazil.
Marcela Souza Lima PauloEscola Superior de Ciências da Santa Casa de Misericórdia de Vitória, Vitória, Brazil.
Paulo A LotufoFaculdade de Medicina FMUSP, Universidade de Sao Paulo, São Paulo, SP, Brazil.
Iolanda de Fátima Lopes Calvo TibérioFaculdade de Medicina FMUSP, Universidade de Sao Paulo, São Paulo, SP, Brazil.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionPollution harms the health of people with asthma. The effect of the anti-inflammatory cholinergic pathway in chronic allergic inflammation associated to pollution is poorly understood.

methodsOne hundred eight animals were divided into 18 groups (6 animals). Groups included: wild type mice (WT), genetically modified with reduced VAChT (VAChTKD), and those sensitized with ovalbumin (VAChTKDA), exposed to metal powder due to iron pelletizing in mining company (Local1) or 3.21 miles away from a mining company (Local2) in their locations for 2 weeks during summer and winter seasons. It was analyzed for hyperresponsivity, inflammation, remodeling, oxidative stress responses and the cholinergic system.

resultsDuring summer, animals without changes in the cholinergic system revealed that Local1 exposure increased the hyperresponsiveness (%Rrs, %Raw), and inflammation (IL-17) relative to vivarium animals, while animals exposed to Local2 also exhibited elevated IL-17. During winter, animals without changes in the cholinergic system revealed that Local2 exposure increased the hyperresponsiveness (%Rrs) relative to vivarium animals. Comparing the exposure local of these animals during summer, animals exposed to Local1 showed elevated %Rrs, Raw, and IL-5 compared to Local 2, while in winter, Local2 exposure led to more IL-17 than Local1. Animals with VAChT attenuation displayed increased %Rrs, NFkappaB, IL-5, and IL-13 but reduced alpha-7 compared to animals without changes in the cholinergic system WT. Animals with VAChT attenuation and asthma showed increased the hyperresponsiveness, all inflammatory markers, remodeling and oxidative stress compared to animals without chronic lung inflammation. Exposure to Local1 exacerbated the hyperresponsiveness, oxidative stressand inflammation in animals with VAChT attenuation associated asthma, while Local2 exposure led to increased inflammation, remodeling and oxidative stress.

conclusionsReduced cholinergic signaling amplifies lung inflammation in a model of chronic allergic lung inflammation. Furthermore, when associated with pollution, it can aggravate specific responses related to inflammation, oxidative stress, and remodeling.

Indexed as

AcetylcholineAsthmaInflammationParticulate matterPollution

Identifiers

PMID38961398
PMCPMC11223391

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.