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Updated: May 25, 2025
Single-cell Analysis of Immunophenotype and Cytokine Production in Peripheral Whole Blood via Mass Cytometry
Published on: June 26, 2018
CD177+ neutrophils exacerbate septic lung injury via the NETs/AIM2 pathway: An experimental and bioinformatics study
Fuquan Wang1, Yan Zhang2, Miaomiao Sun2
1Department of Pain Medicine, China-Japan Friendship Hospital, Beijing, China.
Background:
Acute lung injury (ALI) is one of the most common complications of sepsis. However, the underlying mechanisms and effective treatment strategies remain poorly understood. Immune cells are crucial in sepsis-induced lung injury, yet the heterogeneity of the immune cell populations involved in this context is not well characterized.
Methods:
This study established a Cecal Ligation and Puncture (CLP) mouse model and employed single-cell sequencing along with molecular biology experimental methods to identify the primary functional subgroups of immune cells associated with sepsis-induced ALI, thereby elucidating the key mechanisms related to sepsis-induced ALI.
Results:
Our analysis revealed that, in comparison to normal mice, the top 100 differentially expressed genes (DEGs) in septic lung tissue during the acute phase predominantly originate from neutrophils. Cd177 antigen (Cd177)+ neutrophils represent the predominant subpopulation of neutrophils in septic lung tissue. These cells exhibit unique pro-inflammatory and oxidative stress characteristics, and they are capable of producing excessive neutrophil extracellular traps (NETs). NETs can aggravate ALI by activating Absent in Melanoma 2 (AIM2) inflammasome. Furthermore, we discovered that melatonin could effectively inhibit the infiltration of Cd177+ neutrophils in septic lung tissue, reduce the expression levels of NETs, and diminish the activation of AIM2, thereby improving lung injury.
Conclusion:
Our research provides novel insights and potential therapeutic targets for the treatment of sepsis-induced ALI.
