Evidence map›Paper›PMID 26623095›Full record

ArticleJournal of thoracic disease2015

High mobility group box 1: a novel mediator of Th2-type response-induced airway inflammation of acute allergic asthma.

Libing Ma, Jinrong Zeng, Biwen Mo, Changming Wang, Jianwei Huang, Yabing Sun, Yuanyuan Yu, Shaokun Liu

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of thoracic disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

27 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. AllergoOncology: Role of immune cells and immune proteins.Clinical and translational allergy · 2022
    Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. Resistin family proteins in pulmonary diseases.American journal of physiology. Lung cellular and molecular physiology · 2020
    Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Review
  20. Dihydroartemisinin Ameliorated Ovalbumin-Induced Asthma in Mice via Regulation of MiR-183C.Medical science monitor : international medical journal of experimental and clinical research · 2019
    Article
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 1 institution in 1 country.

Libing Ma1 Department of Respiratory Medicine, the Affiliated Hospital of Guilin Medical University, Guilin 541001, China ; 2 Institute of Respiratory Diseases, Guilin Medical University, Guilin 541001, China ; 3 Key Laboratory of Respiratory Diseases of Colleges and Universities Affiliated Education Department of Guangxi Zhuang Autonomous Region, Guilin 541001, China ; 4 Department of Respiratory Medicine, the Second Xiangya Hospital, Central South University, Changsha 410011, China.
Jinrong Zeng1 Department of Respiratory Medicine, the Affiliated Hospital of Guilin Medical University, Guilin 541001, China ; 2 Institute of Respiratory Diseases, Guilin Medical University, Guilin 541001, China ; 3 Key Laboratory of Respiratory Diseases of Colleges and Universities Affiliated Education Department of Guangxi Zhuang Autonomous Region, Guilin 541001, China ; 4 Department of Respiratory Medicine, the Second Xiangya Hospital, Central South University, Changsha 410011, China.
Biwen Mo1 Department of Respiratory Medicine, the Affiliated Hospital of Guilin Medical University, Guilin 541001, China ; 2 Institute of Respiratory Diseases, Guilin Medical University, Guilin 541001, China ; 3 Key Laboratory of Respiratory Diseases of Colleges and Universities Affiliated Education Department of Guangxi Zhuang Autonomous Region, Guilin 541001, China ; 4 Department of Respiratory Medicine, the Second Xiangya Hospital, Central South University, Changsha 410011, China.
Changming Wang1 Department of Respiratory Medicine, the Affiliated Hospital of Guilin Medical University, Guilin 541001, China ; 2 Institute of Respiratory Diseases, Guilin Medical University, Guilin 541001, China ; 3 Key Laboratory of Respiratory Diseases of Colleges and Universities Affiliated Education Department of Guangxi Zhuang Autonomous Region, Guilin 541001, China ; 4 Department of Respiratory Medicine, the Second Xiangya Hospital, Central South University, Changsha 410011, China.
Jianwei Huang1 Department of Respiratory Medicine, the Affiliated Hospital of Guilin Medical University, Guilin 541001, China ; 2 Institute of Respiratory Diseases, Guilin Medical University, Guilin 541001, China ; 3 Key Laboratory of Respiratory Diseases of Colleges and Universities Affiliated Education Department of Guangxi Zhuang Autonomous Region, Guilin 541001, China ; 4 Department of Respiratory Medicine, the Second Xiangya Hospital, Central South University, Changsha 410011, China.
Yabing Sun1 Department of Respiratory Medicine, the Affiliated Hospital of Guilin Medical University, Guilin 541001, China ; 2 Institute of Respiratory Diseases, Guilin Medical University, Guilin 541001, China ; 3 Key Laboratory of Respiratory Diseases of Colleges and Universities Affiliated Education Department of Guangxi Zhuang Autonomous Region, Guilin 541001, China ; 4 Department of Respiratory Medicine, the Second Xiangya Hospital, Central South University, Changsha 410011, China.
Yuanyuan Yu1 Department of Respiratory Medicine, the Affiliated Hospital of Guilin Medical University, Guilin 541001, China ; 2 Institute of Respiratory Diseases, Guilin Medical University, Guilin 541001, China ; 3 Key Laboratory of Respiratory Diseases of Colleges and Universities Affiliated Education Department of Guangxi Zhuang Autonomous Region, Guilin 541001, China ; 4 Department of Respiratory Medicine, the Second Xiangya Hospital, Central South University, Changsha 410011, China.
Shaokun Liu1 Department of Respiratory Medicine, the Affiliated Hospital of Guilin Medical University, Guilin 541001, China ; 2 Institute of Respiratory Diseases, Guilin Medical University, Guilin 541001, China ; 3 Key Laboratory of Respiratory Diseases of Colleges and Universities Affiliated Education Department of Guangxi Zhuang Autonomous Region, Guilin 541001, China ; 4 Department of Respiratory Medicine, the Second Xiangya Hospital, Central South University, Changsha 410011, China.
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHigh mobility group box 1 (HMGB1) is an inflammatory mediator involved into the advanced stage of systemic inflammatory response syndrome (SIRS), and is over-expressed in bacterial sepsis and hemorrhagic shock. Recently, it has been found that the HMGB1 was abnormally expressed in induced sputum and plasma of asthmatic patients. However, the precise role of HMGB1 in the acute allergic asthma is unclear. Therefore, we aim to investigate the role HMGB1 in regulating airway inflammation of acute allergic asthma and its possible mechanism in this study.

methodsForty-eight BALB/c female mice were randomly divided into four groups: control group (Control), asthma group (Asthma), HMGB1 group (HMGB1) and anti-HMGB1 (HMGB1 monoclonal antibody of mice) group (Anti-HMGB1). Acute allergic asthma mice models were established by ovalbumin (OVA)-challenge. Then, we measured the levels of HMGB1 in bronchoalveolar lavage fluid (BALF) and lung tissue of mice. Finally, after exogenous HMGB1 and/or anti-HMGB1 administration, pulmonary function test, histological analysis, Western blot, cytological analysis and ELISA assay were performed to explore the effect of HMGB1 in acute allergic asthma.

resultsThe levels of HMGB1 in BALF and lung tissue and the expression of HMGB1 protein in the lung tissue of asthma group were significantly higher than those in control group, respectively (P<0.01). Moreover, the HMGB1 group was showed an increased mucus secretion and infiltration of eosinophils and neutrophils in the airway of asthma mice, and a decrease of pulmonary function, compared to control group (P<0.01, respectively). Meanwhile, exogenous HMGB1 could increase the levels of IL-4, IL-5, IL-6, IL-8 and IL-17, whereas could reduce the IFN-γ in the BALF and lung tissue (P<0.05, respectively). Exogenous HMGB1 could enhance GATA3 expression of Th2 cells and attenuate the T-bet expression of Th1 cells (P<0.05, respectively), which could be abrogated after inhibiting HMGB1.

conclusionsHMGB1 could aggravate eosinophilic inflammation in the airway of acute allergic asthma through inducing a dominance of Th2-type response and promoting the neutrophilic inflammation.

Indexed as

acute allergic asthmaeosinophilic airway inflammationHigh mobility group box 1 (HMGB1)neutrophilic airway inflammationTh1/Th2 cells

Identifiers

PMID26623095
PMCPMC4635276
OpenAlexW1908323924

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.