Evidence map›Paper›PMID 32400128›Full record

ArticleAllergy, asthma & immunology research2020

Toll-like Receptor 4 Deficiency Aggravates Airway Hyperresponsiveness and Inflammation by Impairing Neutrophil Apoptosis in a Toluene Diisocyanate-Induced Murine Asthma Model.

Shuyu Chen, Yao Deng, Qiaoling He, Yanbo Chen, De Wang, Weimin Sun, Ying He, Zehong Zou, Zhenyu Liang, Rongchang Chen and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Allergy, asthma & immunology research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Distinct single-cell transcriptional profile in CD4+ T-lymphocytes among obese children with asthma.American journal of physiology. Lung cellular and molecular physiology · 2025
    Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Is TLR4 Critical for Neutrophil Apoptosis in Occupational Asthma?Allergy, asthma & immunology research · 2020
    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

12 authors.

Shuyu Chen *The Second Affiliated Hospital, Guangdong Provincial Key Laboratory of Allergy & Clinical Immunology, State Key Laboratory of Respiratory Disease, Guangzhou Medical University, Guangzhou, China.ORCID https://orcid.org/0000-0002-8068-649X
Yao Deng *The Second Affiliated Hospital, Guangdong Provincial Key Laboratory of Allergy & Clinical Immunology, State Key Laboratory of Respiratory Disease, Guangzhou Medical University, Guangzhou, China.ORCID https://orcid.org/0000-0002-3741-1933
Qiaoling He *The Second Affiliated Hospital, Guangdong Provincial Key Laboratory of Allergy & Clinical Immunology, State Key Laboratory of Respiratory Disease, Guangzhou Medical University, Guangzhou, China.ORCID https://orcid.org/0000-0003-3141-3986
Yanbo ChenGuangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, China.ORCID https://orcid.org/0000-0002-5163-6506
De WangThe Second Affiliated Hospital, Guangdong Provincial Key Laboratory of Allergy & Clinical Immunology, State Key Laboratory of Respiratory Disease, Guangzhou Medical University, Guangzhou, China.ORCID https://orcid.org/0000-0001-8586-4593
Weimin SunThe Second Affiliated Hospital, Guangdong Provincial Key Laboratory of Allergy & Clinical Immunology, State Key Laboratory of Respiratory Disease, Guangzhou Medical University, Guangzhou, China.ORCID https://orcid.org/0000-0001-9504-031X
Ying HeThe Second Affiliated Hospital, Guangdong Provincial Key Laboratory of Allergy & Clinical Immunology, State Key Laboratory of Respiratory Disease, Guangzhou Medical University, Guangzhou, China.ORCID https://orcid.org/0000-0002-3903-3868
Zehong ZouThe Second Affiliated Hospital, Guangdong Provincial Key Laboratory of Allergy & Clinical Immunology, State Key Laboratory of Respiratory Disease, Guangzhou Medical University, Guangzhou, China.ORCID https://orcid.org/0000-0002-8532-3559
Zhenyu LiangState Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.ORCID https://orcid.org/0000-0002-8746-315X
Rongchang ChenState Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.ORCID https://orcid.org/0000-0002-2396-3702
Lihong YaoState Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital, Guangzhou Medical University, Guangzhou, China. yaolh4321@126.com.ORCID https://orcid.org/0000-0002-3267-5980
Ailin TaoThe Second Affiliated Hospital, Guangdong Provincial Key Laboratory of Allergy & Clinical Immunology, State Key Laboratory of Respiratory Disease, Guangzhou Medical University, Guangzhou, China.ORCID https://orcid.org/0000-0002-0584-921X

Funding

Guangzhou Healthcare Collaborative Innovation Major Project 201604020012National Key R&D Program of China 2017YFC1310601National Natural Science Foundation of China 81800022National Natural Science Foundation of China 81871266Scientific and Technological Project of Guangzhou 201604020008Scientific and Technological Project of Guangzhou 201804020042
6 · The paper itself

Abstract

purposeAccumulating evidence has suggested that toll-like receptor 4 (TLR4) is critically involved in the pathogenesis of asthma. The aim of this study was to investigate the role of TLR4 in toluene diisocyanate (TDI)-induced allergic airway inflammation.

methodsTLR4

resultsTDI exposure led to increased airway hyperresponsiveness (AHR), granulocyte flux, bronchial epithelial shedding and extensive submucosal collagen deposition, which were unexpectedly aggravated by TLR4 deficiency. Following TDI challenge, TLR4

conclusionsThese data indicated that TLR4 deficiency promoted neutrophil infiltration by impairing its apoptosis via up-regulation of Bcl-2, thereby resulting in deteriorated AHR and airway inflammation, which suggests that TLR4 could be a negative regulator of TDI-induced neutrophilic inflammation.

Indexed as

apoptosisasthmaneutrophlic inflammationToll-like receptor 4toluene diisocyanate

Identifiers

PMID32400128
PMCPMC7225000

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.