AI Article Synopsis
- NK cells play a crucial role in the immune response during sepsis-induced ARDS, but their specific characteristics in this condition are not well understood.
- A study of 115 septic patients showed that those with ARDS had significantly lower NK cell percentages, which correlated with higher mortality rates compared to those with sepsis alone.
- Unique MX1NK cells were identified in ARDS patients, characterized by their response to type I interferons, suggesting they may contribute to severe inflammation and indicating their potential as a therapeutic target.
Article Abstract
Background: Natural killer (NK) cells are key regulators of immune defense in sepsis-induced acute respiratory distress syndrome (ARDS), yet the characteristics of NK cell clusters in ARDS remain poorly understood.
Methods: A prospective and observational study enrolled septic patients with ARDS or not was conducted to determine the percentage of NK cells via flow cytometry. The transcriptomes of peripheral blood mononuclear cells (PBMCs) from healthy controls, patients with sepsis only, and patients with sepsis-induced ARDS were profiled. Vitro experiments were performed to confirm the mechanism mediating MX1NK cell infiltration.
Results: A total of 115 septic patients were analyzed, among whom 63 patients developed ARDS and 52 patients did not. Decreased NK percentages were found in sepsis with ARDS patients (%, 7.46±4.40 vs 11.65±6.88, P=0.0001) compared with sepsis-only patients. A lower percentage of NK cells showed a significant increase in 28-day mortality. Single-cell sequencing analysis revealed distinct characteristics of NK cells in sepsis-induced ARDS, notably the identification of a unique cluster defined as MX1NK cells. Flow cytometry analysis showed an elevated percentage of MX1NK cells specifically in individuals with sepsis-induced ARDS, compared with patients with sepsis only. Pseudo-time analysis showed that MX1NK cells were characterized by upregulation of type I interferon-induced genes and other pro-inflammatory genes. MX1NK cells can respond to type I interferons and secrete type I interferons themselves. Ligand-receptor interaction analysis also revealed extensive interaction between MX1NK cells and T/B cells, leading to an uncontrolled inflammatory response in ARDS.
Conclusion: MX1NK cells can respond to type I interferons and secrete type I interferons themselves, promoting the development of sepsis-induced ARDS. Interfering with the infiltration of MX1NK cells could be a therapeutic approach for this disease. Due to the limited sample size, a larger sample size was needed for further exploration.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11110828 | PMC |
| http://dx.doi.org/10.2147/JIR.S460259 | DOI Listing |
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