Abstract
Pressure ulcers (PUs) result from prolonged pressure and shear forces, which cause local skin and soft tissue injury. Elderly patients with pressure injuries face a higher risk of death. Diabetes presents a significant comorbid condition that increases the risk of PU development due to underlying neuropathy, vasculopathy, and impaired wound healing. Recent molecular biology research on PU subjects has identified inappropriate responses to inflammatory stressors as a significant risk factor. Systemic manifestations, such as an increased abundance of inflammatory cells and alterations in inflammatory mediators, have been linked to PU formation. The present study adopted a bioinformatics, multi-omic data-mining approach to understand cellular and molecular dysregulation and identify biomarkers that may guide the development of more effective screening, diagnostic, and therapeutic strategies in the management of severe PU subjects. At the RNA level, differential gene expression indicated T cell dysfunction and impaired T cell communication in severe PU subjects. Protein-based analysis further validated this finding, as T lymphocyte functional readouts, such as Th1 cell response, memory T cell activation, and Th17 cell differentiation, were predicted to be downregulated. Taken together, our results show that T lymphocyte function and communication remain impaired in severe PU and could guide the development of a therapeutic cell-based treatment for regenerative medicine.