Changes in ferroptosis-related molecular expression in macrophages of community-acquired pneumonia patients and their associated with the disease progression
Abstract
OBJECTIVE: To investigate the expression of ferroptosis-related molecules in macrophages of community-acquired pneumonia (CAP) patients and explore their association with disease severity. This study provides novel insights into the role of ferroptosis in CAP pathogenesis by integrating transcriptome sequencing, RT-qPCR, Western blot, and flow cytometry analyses. METHODS: Ferroptosis-related molecules were analyzed in CD14⁺ monocytes and CD11b⁺ macrophages from CAP patients using transcriptome sequencing, RT-qPCR, Western blot, and flow cytometry. Clinical data from CAP patients (n = 46) and healthy controls (n = 63) were compared. RESULTS: CAP patients exhibited elevated levels of ferroptosis markers (PTGS2, Fe²⁺, and lipid peroxides) and downregulation of inhibitors (TP53 and GPX4). Transcriptome analysis showed activation of the ferroptosis pathway, with significant changes correlating with disease severity. Elevated neutrophil counts and decreased lymphocyte levels were also observed in CAP patients. CONCLUSION: Ferroptosis is intricately involved in CAP pathogenesis, with altered expression of key molecules contributing to disease progression. Our findings highlight the potential of targeting ferroptosis-related molecules (e.g., TP53, GPX4, and PTGS2) as a novel therapeutic strategy to mitigate inflammation and tissue damage in CAP. Future studies should validate these findings in larger cohorts.
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