Abstract
INTRODUCTION: Burn injuries lead to dysregulation of immune molecules, impacting cellular and humoral immune pathways. This study aims to determine the prediction of immune molecule activity during burn wound healing among elderly patients. METHODS: The current study utilized the Gene Expression Omnibus (GEO) database to extract the proper gene set. Also, the literature review was conducted in the present study to find immune signatures. The study used the "enrich r" website to identify the biological functions of extracted genes. The critical gene modules related to mortality were identified using the weighted gene co-expression network analysis (WGCNA) R package. RESULTS: The appreciated GSE was extracted. According to the data, the most upregulated signatures were related to natural killer (NK) cells, and the most downregulated signatures were associated with M1 macrophages. Also, the results of WGCNA have shown that the most related gene modules (P<107 and score 0.17) to mortality were investigated, and the modules 100 first genes were extracted. Additionally, the enrich r analysis has demonstrated related pathways, including the immune process, including regulation of histamine secreted from mast cell (P<0.05), T helper 17 cell differentiation (P<0.05), and autophagy (P<0.05) were obtained. Finally, by network analysis, the critical gene "B3GNT5" were obtained (degree>ten and "betweenness and centrality">30 were considered). CONCLUSION: The study identified significant changes in macrophage and NK cell expression patterns post-burn injury, linking them to potential improvements in clinical outcomes and wound healing. The gene B3GNT5, associated with mortality, was highlighted as a key marker for prognostic evaluation.