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Published in: Inflammation 5/2022

19-04-2022 | Acute Respiratory Distress-Syndrome | Original Article

The Effect and Mechanism of Lipoxin A4 on Neutrophil Function in LPS-Induced Lung Injury

Authors: Wen-Hao Pan, Xin Hu, Ben Chen, Qi-Chao Xu, Hong-Xia Mei

Published in: Inflammation | Issue 5/2022

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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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Metadata
Title
The Effect and Mechanism of Lipoxin A4 on Neutrophil Function in LPS-Induced Lung Injury
Authors
Wen-Hao Pan
Xin Hu
Ben Chen
Qi-Chao Xu
Hong-Xia Mei
Publication date
19-04-2022
Publisher
Springer US
Published in
Inflammation / Issue 5/2022
Print ISSN: 0360-3997
Electronic ISSN: 1573-2576
DOI
https://doi.org/10.1007/s10753-022-01666-5

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