ArticleInflammation2022
The Effect and Mechanism of Lipoxin A4 on Neutrophil Function in LPS-Induced Lung Injury.
Article in Inflammation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 23 citations in OpenAlex.
- Endoplasmic reticulum stress exacerbates ischemia-reperfusion-induced pulmonary endothelial barrier dysfunction by activating TXNDC5.Journal of advanced research · 2026Article
- Endogenous Lipid Signals in Energy Homeostasis and Fibrosis.Biomolecules · 2026Review
- The IL-12 family cytokines in neurodegenerative diseases: dual roles in neurotoxicity and neuroprotection.Inflammopharmacology · 2025Review
- Advances in acute respiratory distress syndrome: focusing on heterogeneity, pathophysiology, and therapeutic strategies.Signal transduction and targeted therapy · 2025Review
- TheFrontiers in immunology · 2025Review
- Treatment with lipoxin AInflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- Association between arachidonate lipoxygenase 15,c.-292 C > T gene polymorphism and non-cystic fibrosis bronchiectasis in children: a pilot study on the effects on airway lipoxin A4 and disease phenotype.Italian journal of pediatrics · 2024Article
- Inflammasome activity regulation by PUFA metabolites.Frontiers in immunology · 2024Review
- Lipoxin A4 Ameliorates Imiquimod-Induced Psoriasis-Like Dermatitis via Promoting the Regression of Inflammation.Clinical, cosmetic and investigational dermatology · 2023Article
- The protective effects of lipoxin A4 on type 2 diabetes mellitus: A Chinese prospective cohort study.Frontiers in endocrinology · 2023Article
- Eicosanoids in inflammation in the blood and the vessel.Frontiers in pharmacology · 2022Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Excessive inflammatory response caused by infiltration of a large number of neutrophils is one of the important features of acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). Lipoxin A4 (LXA4) is an important endogenous mediator in the process of inflammation resolution, which has a strong role in promoting inflammation resolution. In this study, we examined the impact of LXA4 on the pulmonary inflammatory response and the neutrophil function in ARDS rats. Our results indicated that exogenous administration of LXA4 could reduce the degree of lung injury in ARDS rats and inhibit the release of pro-inflammatory factors TNF-α and IL-1β in lung tissue homogenate. However, LXA4 has no lung protective effect on ARDS rats of neutropenia, nor can it inhibit the levels of pro-inflammatory factors TNF-α and IL-1β in lung tissue homogenate. LXA4 can inhibit the production of reactive oxygen species (ROS) and neutrophil extracellular traps (NETs) in peripheral blood neutrophils of ARDS rats. At the same time, LXA4 can promote the phagocytosis of neutrophils in ARDS rats in vitro and can also promote the apoptosis of neutrophils in ARDS rats. In addition, the effect of LXA4 on the function of neutrophils in ARDS rats is mediated by its receptor ALX. LXA4 can inhibit the release of NE and MPO from neutrophils, thereby reducing the production of NETs. In summary, these findings indicate that LXA4 has a protective effect on LPS-induced ARDS rats by affecting the function of neutrophils.
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