Unveiling the molecular mechanisms of burn injury through integrated single-cell and bulk transcriptomic analysis.

purposeBurn injuries are prevalent and have a significant effect on patients' quality of life and healthcare costs. Current treatment modalities, such as wound care and surgical interventions, often face challenges due to complications like infection and inadequate healing.

methodsThis study adopted single-cell RNA sequencing (scRNA-seq) to investigate the cellular landscape of the burn microenvironment. After rigorous quality control filtering, 9,248 cells were retained for analysis. Using UMAP dimensionality reduction, these cells were annotated into 14 subpopulations, including Neutrophils, Macrophages, and T cells. Differential gene analysis and machine learning techniques, such as LASSO regression and random forest selection, were employed to identify marker genes.

resultsMacrophages exhibited significant interactions with other cell types, indicating their pivotal role in immune signaling within the burn microenvironment. A total of 155 genes were identified as markers for Macrophages, with AP2A2, CCL7, and TF emerging as key features. Immune infiltration analysis also revealed notable differences in the proportions of immune cells, particularly Mast cells and Neutrophils, highlighting on their involvement in disease progression.

conclusionThis study provides novel insights into the immunological microenvironment of burn injuries. Despite limitations including a modest sample size and lack of experimental validation, our findings establish a foundation for future investigations into targeted immunotherapeutic strategies, potentially improving clinical outcomes and advancing personalized treatment approaches for burn patients.