Ozone therapy: A new breath of life for sepsis-induced lung injury

Published On 2025-01-09 15:45 GMT   |   Update On 2025-01-09 15:45 GMT

A cutting-edge study has identified medical ozone therapy as a promising new treatment for sepsis-induced acute lung injury (ALI). By enhancing the clearance of neutrophil extracellular traps (NETs) through the AMP-activated protein kinase (AMPK)/scavenger receptor A1 (SR-A1) pathway, this innovative approach could significantly improve survival rates and lung function in preclinical models, offering hope for patients with limited treatment options.

Sepsis, a severe and often fatal complication of infection, is a leading cause of both ALI and acute respiratory distress syndrome (ARDS). These conditions, which are associated with high mortality rates, remain challenging to treat due to the lack of effective therapies. NETs play a central role in the progression of sepsis, as they are involved in trapping pathogens but can also trigger excessive inflammation, exacerbating lung injury. The complexity of sepsis-induced ALI, driven by the interplay among inflammation, immune dysregulation, and coagulation, calls for innovative therapeutic strategies to better manage this critical condition.

In a study from Nanjing Medical University, researchers have made significant progress in this area. Published in the Journal of Biomedical Research on November 28, 2024, the study details how medical ozone therapy targets the AMPK/SR-A1 axis to effectively clear NETs, significantly improving survival rates and lung function in mice suffering from sepsis-induced ALI. This work represents a critical step forward in the search for new treatments for this deadly condition.

The study provides an in-depth examination of the mechanisms behind ozone therapy's therapeutic effects on sepsis-induced ALI. Researchers discovered that ozone treatment reduced the formation of NETs, which was a key factor in the development of ALI. By activating the AMPK/SR-A1 pathway, ozone therapy enhanced the ability of macrophages to clear these harmful NETs, reducing inflammation and mitigating lung injury. The research also emphasizes the essential role of SR-A1: in knockout mice lacking SR-A1, ozone therapy failed to produce its protective effects, highlighting the receptor's critical role in mediating ozone's therapeutic impact. A comprehensive evaluation of lung function, blood flow, and protein levels further demonstrated the multifaceted benefits of ozone treatment, suggesting that it could become a valuable addition to existing therapies for sepsis-induced ALI.

Dr. Wen-Tao Liu, the principal investigator of the study, underscores the significance of these findings: Our research demonstrates that medical ozone therapy could dramatically improve the management of sepsis-induced ALI. By activating the AMPK/SR-A1 pathway, ozone therapy clears harmful NETs, restores immune balance, and reduces inflammation. This represents a promising new approach to critical care that could lead to better outcomes for patients suffering from sepsis.

The implications of this study are far-reaching. If subsequent research confirms these results in human trials, medical ozone therapy could become a viable and effective treatment for sepsis-induced lung injury, a condition currently with few treatment options. Ozone therapy's potential to improve survival and lung function could transform the management of sepsis, offering new hope for patients who face a bleak prognosis. As this promising therapy advances through further research, it may become a cornerstone in the fight against sepsis, reshaping how we treat this life-threatening condition.

Reference:

Chenxiao Yan, Yong Zhang, Lai Jin, Xiaojie Liu, Xuexian Zhu, Qifeng Li, Yu Wang, Liang Hu, Xueming He, Hongguang Bao, Xia Zhu, Qian Wang, Wen-Tao Liu. Medical ozone alleviates acute lung injury by enhancing phagocytosis targeting NETs via AMPK/SR-A1 axis[J]. The Journal of Biomedical Research, 2024, 38(6): 569-584. DOI: 10.7555/JBR.38.20240038

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Article Source : Journal of Biomedical Research

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