PubMed · 10090393
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1999. Recent references.. https://pubmed.ncbi.nlm.nih.gov/10090393/
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BACKGROUND: Burn injuries trigger complex immune responses and gene expression changes, impacting wound healing and systemic inflammation. Understanding these changes is crucial for identifying biomarkers and therapeutic targets. METHODS: We analyzed two gene expression omnibus datasets (wound tissue [GSE8056] and blood [GSE37069]) to identify differentially expressed genes (DEGs) in burn injury samples versus controls. Immune cell proportions were assessed using CIBERSORT. Functional enrichment analyses (Gene Ontology and Kyoto Encyclopedia of Genes and Genomes) and protein-protein interaction networks were constructed to identify key genes and pathways. RESULTS: We identified 1170 upregulated and 1227 downregulated DEGs. Gene Ontology analysis revealed enrichment in neutrophil activation, inflammatory response, and extracellular matrix organization. Kyoto Encyclopedia of Genes and Genomes analysis highlighted cytokine-cytokine receptor interaction, TNF, and IL-17 signaling pathways. Immune infiltration analysis showed significant changes in neutrophils, macrophages (M1/M2), and T-cell subsets. Protein-protein interaction network analysis identified five hub genes: JUN, STAT1, Bcl2, MMP9, and TLR2. CONCLUSIONS: This study provides a comprehensive bioinformatic analysis of gene expression and immune responses in burn injuries. The identified DEGs, hub genes, and pathways offer insights into the immune response mechanisms and suggest potential targets for diagnostic and therapeutic interventions in burn injury management.
Even in the absence of inhalational injury, acute lung injury is a common cause of morbidity and mortality for patients sustaining severe burns. Other than general supportive measures, there are few therapeutic options for improving survival in these critically ill patients. Numerous clinical and laboratory studies have implicated tumor necrosis factor (TNF)-a and neutrophils as important participants in the pathogenesis of burn-induced lung injury. There is, however, little information regarding the mechanism by which these and other pro-inflammatory mediators affect the movement of fluid and protein across the microvascular barrier into the interstitium of the lung. In addition to reviewing the evidence implicating TNF-a and neutrophils in the pathophysiology of burn-induced lung injury, this report summarizes current theories regarding potential mechanisms by which these mediators may alter microvascular barrier function to lead ultimately to the development of pulmonary edema.
Although excision and grafting of burns has become common and standard, many surgeons have been reluctant to excise and graft face burns. In fact, we could find photographic results at 1 year after grafting of only eight patients in the English literature. We began excision and grafting of face burns in 1979 and presented our first 16 patients in 1986 in this journal. With encouragement from Janzekovic and Jackson, we continued and have now used essentially the same procedure for more than 20 years in approximately 100 patients and, from this large series, are able to present outcomes. From January of 1979 to May of 1999, we performed excision and grafting on 91 patients with deep face burns. Data were recorded and 35-mm photographs were obtained throughout the 20-year period. We reviewed that database and the slide files of these patients. We found 45 patients with complete photographic sets including 1-year follow-up. Since, in our opinion, there is no useful, objective measure of appearance, we decided to simply publish all 45 sets of complete photographs, permitting the reader to subjectively form an opinion of the outcome of this procedure. The results are all shown as "full" face burns and two "partial" face burns. We continue to believe that early excision and grafting is indicated for face burns that will not heal within 3 weeks and that the procedure yields results that permit the burn victims to return to society and minimizes the time off work or out of school.