Evidence map›Paper›PMID 40963601›Full record

ArticleFrontiers in immunology2025

The role of neutrophils and NETosis in lipopolysaccharide exacerbated asthmatic airway inflammation.

Qian Qian, Qianye Zhao, Yongji Qian, Huan Deng, Xiaoming Feng, Jiamin Zhang, Xia Huang, Yi Du, Deyu Zhao, Feng Liu

Abstract read
In one paragraph

Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Gngt2 promotes inflammatory dendritic cell programming through an ATG5-NF-κB signaling axis in neutrophilic asthma.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    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

10 authors.

Qian QianDepartment of Respiratory Medicine, Children's Hospital of Nanjing Medical University, Nanjing, China.
Qianye ZhaoDepartment of Respiratory Medicine, Lianyungang Maternal and Child Health Hospital, Lianyungang, China.
Yongji QianDepartment of Respiratory Medicine, Children's Hospital of Nanjing Medical University, Nanjing, China.
Huan DengDepartment of Respiratory Medicine, Children's Hospital of Nanjing Medical University, Nanjing, China.
Xiaoming FengDepartment of Traditional Chinese Medicine, Lianyungang Traditional Chinese Medicine Branch of Jiangsu Union Technical Institute, Lianyungang, China.
Jiamin ZhangDepartment of Respiratory Medicine, Children's Hospital of Nanjing Medical University, Nanjing, China.
Xia HuangDepartment of Respiratory Medicine, Children's Hospital of Nanjing Medical University, Nanjing, China.
Yi DuDepartment of Respiratory Medicine, Lianyungang Maternal and Child Health Hospital, Lianyungang, China.
Deyu ZhaoDepartment of Respiratory Medicine, Children's Hospital of Nanjing Medical University, Nanjing, China.
Feng LiuDepartment of Respiratory Medicine, Children's Hospital of Nanjing Medical University, Nanjing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Lipopolysaccharides (LPS) are associated with the exacerbation of asthma, accompanied by an increased recruitment of neutrophils to the airway. The role of these neutrophils warrants thorough investigation. Methods: In this study, three genotypes of mice were utilized to establish an asthma model aggravated by LPS combined with ovalbumin (OVA). The bronchoalveolar lavage fluid (BALF) of mice was obtained to detect neutrophil-related inflammatory factors. Lung tissues were collected for staining, and neutrophils derived from bone marrow of mice were subjected to transcriptomic sequencing analysis. Results: Our findings revealed that, compared to eosinophilic asthma, Exacerbated asthma triggered by LPS combined with OVA showed more severe airway inflammation. Neutrophil-related markers like IL6, IL8, and neutrophil extracellular traps (NETs) were significantly elevated in this model. Inhibiting neutrophils production significantly improved airway inflammation and lung function. Analysis of differentially expressed genes (DEGs) in bone marrow neutrophils highlighted enrichment in the NETs pathway. Suppressing NETs yielded similar results to decreasing neutrophils. Conclusion: Our results indicate that NETs are involved in the pathogenesis of LPS exacerbated asthmatic airway inflammation, and targeting the NETosis function of neutrophils may represent an effective therapeutic approach.

Indexed as

AsthmaExtracellular TrapsLipopolysaccharidesNeutrophilsAnimalsBronchoalveolar Lavage FluidDisease Models, AnimalFemaleInflammationLungMiceOvalbuminLipopolysaccharidesOvalbuminairway inflammationdifferentially expressed geneslipopolysaccharideneutrophil extracellular trapsneutrophilic asthma

Identifiers

PMID40963601
PMCPMC12436110

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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.