REVIEW article
Front. Immunol.
Sec. Inflammation
Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1556923
Friend or foe: the role of platelets in acute lung injury
Provisionally accepted
- 1School of Integrative Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin, China
- 2Department of Thoracic and Cardiovascular Surgery, Hua Shan Hospital, Affiliated with Fudan University, Shanghai, China
- 3Huashan Hospital, Fudan University, Shanghai, Shanghai Municipality, China
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Lung diseases, including acute lung injury (ALI) and acute respiratory distress syndrome (ARDS), are associated with various etiological factors and are characterized by high mortality rates. Current treatment strategies primarily focus on lung-protective ventilation and careful fluid management.Despite over 50 years of basic and clinical research, effective treatment options remain limited, and the search for novel strategies continues. Traditionally, platelets have been viewed primarily as contributors to blood coagulation; however, recent research has revealed their significant role in inflammation and immune regulation. While the relationship between platelet count and ALI/ARDS has remained unclear, emerging studies highlight the "dual role" of platelets in these conditions. On one hand, platelets interact with neutrophils to form neutrophil extracellular traps (NETs), promoting immune thrombosis and exacerbating lung inflammation. On the other hand, platelets also play a protective role by modulating inflammation, promoting regulatory T cell (Treg) activity, and assisting in alveolar macrophage reprogramming. This dual functionality of platelets has important implications for the pathogenesis and resolution of ALI/ARDS. This review examines the multifaceted roles of platelets in ALI/ARDS, focusing on their immunomodulatory effects, the platelet-neutrophil interaction, and the critical involvement of platelet-Treg cell complexes in shaping the inflammatory environment in ALI.
Keywords: ALI/ARDS, platelets, Inflammation, Immune Regulation, Neutrophil, Regulatory T Cell
Received: 07 Jan 2025; Accepted: 24 Apr 2025.
Copyright: © 2025 Yang, Zhou, Qiao and Shi. 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: Meng Shi, Department of Thoracic and Cardiovascular Surgery, Hua Shan Hospital, Affiliated with Fudan University, Shanghai, China
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.