Evidence map›Paper›PMID 28391514›Full record

ArticleInflammation2017

Inflammatory and Oxidative Stress Markers in Experimental Allergic Asthma.

Renata Tiscoski Nesi, Emanuel Kennedy-Feitosa, Manuella Lanzetti, Mariana Barcellos Ávila, Clarissa Bichara Magalhães, Walter Araújo Zin, Débora Souza Faffe, Luís Cristóvão Porto, Samuel Santos Valença

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

10 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Therapeutic Effect of Bilsaan,Oxidative medicine and cellular longevity · 2020
    Article
  6. Article
  7. Article
  8. Article
  9. Protective Effects of Casticin FromFrontiers in pharmacology · 2018
    Article
  10. Animal models of asthma: utility and limitations.Journal of asthma and allergy · 2017
    Review
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

9 authors at 4 institutions in 1 country.

Renata Tiscoski NesiInstituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil. retiscoski@gmail.com.
Emanuel Kennedy-FeitosaInstituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Manuella LanzettiInstituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Mariana Barcellos ÁvilaInstituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Clarissa Bichara MagalhãesInstituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Walter Araújo ZinInstituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Débora Souza FaffeInstituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Luís Cristóvão PortoPrograma de Pós-graduação em Biologia Humana e Experimental, Universidade do Estado do Rio de Janeiro, Rio de Janeiro, Brazil.
Samuel Santos ValençaInstituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Universidade Federal do Rio de Janeiro · BRUniversidade de Fortaleza · BRUniversidade do Estado do Rio de Janeiro · BRUniversidade do Extremo Sul Catarinense · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ovalbumin-induced allergic lung inflammation (ALI) is a condition believed to be mediated by cytokines, extracellular matrix remodeling, and redox imbalance. In this study, we evaluated pulmonary function together with inflammatory markers as interleukin-4 (IL-4), myeloperoxidase (MPO), eosinophil cells, and redox markers in the lungs of BALB/c mice after ovalbumin (OVA) sensitization and challenge. Our results showed an increase in bronchial hyperresponsiveness stimulated by methacholine (Mch), inflammatory cell influx, especially eosinophils together with an increase of high mobility group box 1 (HMGB1) and altered lipid peroxidation (LP) and antioxidant defenses in the OVA group compared to the control group (p ≤ 0.5). Thus, we demonstrated that OVA-induced ALI altered redox status concomitantly with impaired lung function, which was associated with HMGB1 expression and proteolytic remodeling. Taken together all results found here, we may suggest HMGB1 is an important therapeutic target for asthma, once orchestrates the redox signaling, inflammation, and remodeling that contribute to the disease development.

Indexed as

InflammationOxidative StressAnimalsAsthmaBiomarkersBronchial HyperreactivityEosinophilsHMGB1 ProteinLipid PeroxidationMiceMice, Inbred BALB COvalbuminProteolysisBiomarkersHMGB1 ProteinOvalbuminasthmaHMGB1inflammationoxidative stresspulmonary mechanics

Identifiers

PMID28391514
OpenAlexW2604643704

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.