ORIGINAL RESEARCH article
Front. Immunol.
Sec. Inflammation
Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1651085
This article is part of the Research TopicNeutrophils in Allergic DiseaseView all articles
The role of neutrophils and NETosis in lipopolysaccharide exacerbated asthmatic airway inflammation
Provisionally accepted- 1Lianyungang Maternal and Children’s Hospital, Lianyungang, China
- 2Children's Hospital of Nanjing Medical University, Nanjing, China
- 3Lianyungang Traditional Chinese Medicine Branch of Jiangsu Union Technical Institute, lianyungang, China
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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.
Keywords: lipopolysaccharide, Neutrophilic asthma, neutrophil extracellular traps, Differentially expressed genes, airway inflammation
Received: 20 Jun 2025; Accepted: 19 Aug 2025.
Copyright: © 2025 Qian, Qian-ye, Deng, Feng, Zhang, Huang, Du, Zhao and Liu. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Feng Liu, Children's Hospital of Nanjing Medical University, Nanjing, China
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