The Major role of TNF-α and miR-203 in the Immune Response of Diabetic Foot Ulcer

Background: Diabetic foot ulcers (DFUs) are a major complications of diabetes mellitus, often complicated by infections particularly with Pseudomonas aeruginosa, a pathogen known to impair wound healing. Tumor necrosis factor-alpha (TNF-α) is a key inflammatory mediator and microRNA-203 (miR-203) has been suggested to play a role in regulating immune responses and inflammation. However, the interactions between Pseudomonas aeruginosa, TNF-α and miR-203 in DFUs remain poorly understood. Objective: This study was designed to explore the correlation between Pseudomonas aeruginosa infection and polymorphism (miR-203 and TNF-α) in a cohort of diabetic patients with foot ulcers. Methodology: The study involved the collection of 210 samples which were categorized based on sex (male and female) and geographic location (Urban and Rural). The following tests were conducted: Complete Blood Count (CBC), C-Reactive Protein (CRP), Erythrocyte Sedimentation Rate (ESR), and HbA1c. Afterward, DNA was extracted from whole blood samples. Immunological assays were performed to measure TNF-α, and miR-203 polymorphisms. Additionally, 70 samples from diabetic foot patients were examined to detect Pseudomonas aeruginosa using biochemical tests, with confirmation achieved through the VITEK2 system compact. Results: A total of 210 diabetic person included 70 healthy control, 70 DM without foot ulcers and 70 DM with foot ulcer through August 2022 to April 2023. In this study TNF-α polymorphism in healthy controls and DM without foot ulcer were (GG and AA(0) while the AG (70) ) while TNF-α polymorphism in DFU (GG 4 , AA 7 and AG 59) and (G 67 and A 73). The P. value (0.310) in Micro-RNA with healthy control, the P. value (<0.001) in Micro-RNA with DM without foot ulcer and DFUs. Conclusion: The findings suggest that miR-203 could serve as a potential therapeutic target for modulating inflammation and improving wound healing in DFUs. Additionally, TNF-α may represent a key mediator in the inflammatory pathway that links infection to impaired wound recovery.