The Preliminary Research On The Interaction Of Diabetic Foot Infection And Autophagy

Objective:1. To analyze the clinical characteristics of patients with diabetic foot infection(DFI) and foot infection but without diabetes. 2. By compared with the level of cell autophagy expression in wound granulation tissue of paitients with foot infection but not mergered with diabetes, to discuss the influence of diabetes mellitus(DM) on cell autophagy expression and whether the level of cell autophagy is different when mergered with pseudomonas aeruginosa infection. In addition, to research the effect of ischemia on the autophagy for diabetic foot infection paitients.Methods: A total of 90 patients diagnosed with DFI hospitalized in Metabolic Hospital of Tianjin Medical University(Diabetes group, DG) and 51 patients diagnosed with foot infection but without DM(Control group, CG) from June 2014 to November 2015 were enrolled. The clinical data of the patients were recorded in detail. We need to analyze the clinical characteristics of patients. The distribution characteristics of bacterias, the positive rate of pseudomonas aeruginosa(PA) and multi-drug resistant pseudomonas aeruginosa(MDRPA) in two groups were analyzed based on the results of bacterial culture and antimicrobial susceptibility. 2. The granulation tissue have been obtained after infection wound debridement and made paraffin section for patients with foot infection in two groups. Firstly, the pathology change of granulation tissue between the two groups was compared by means of HE dyeing. Secondly, the autophagy marker protein microtubule associated protein1 light chain 3-II(LC3-II) and the autophagy positive regulatory protein Beclin-1 were detected in two groups by immunohistochemistry staining. According to the result of immunohistochemical analysis, the level of cell autophagy of granulation tissue was compared, especially merged with pseudomonas aeruginosa infection. The influence of ischemia on cell autophagy was also analyzed for patients with diabetic foot infection. In the end, the immunofluorescence double staining was initiated to detedct CD14(the macrophage marker) and protein LC3-II(autophagy marker) to analyz the level of macrophage autophagy in the two groups.Results:1. No differences were found between the two groups in the age, gender, ulcer size, body mass index, hypertension, coronary heart disease, cerebrovascular disease and lipid metabolic disorder(P > 0.05). However, the glycated hemoglobin a of patients in DG were significantly higher than CG(P < 0.05). In terms of inflammatory markers: there were no differences were observed in the percentage of neutrophil and blood sedimentation in the two groups, but compared with the CG(P > 0.05), the count of white blood cell was obviously lower and c-reactive protein was significantly higher in DG(P < 0.05). A total of 105 in DM group and 71 strains of pathogens were detected, and the main pathogens were gram positive bacterias(59.0% in DG, 57.7% in CG). No changes were found between the two groups in the distribution and species of bacterias(P > 0.05). In addition, gram-positive bacterias were given priority to with staphylococcus aureus and pseudomonas aeruginosa gram-negative bacteria held an important position in gram negative bacterias. The resistance rate of antibiotics of pseudomonas aeruginosa were also high both in the two groups. Higher percentage of the detection of MDRPA were found in DG compared with CG. 2. Compared with CG, the numbers of blood capillary and inflammatory cells in granulation tissue, the quantity of positive staining cells of the detect of LC3-II and Beclin-1 of all patients, and the expressions of positive staining cells of LC3-II and Beclin-1 of patients with pseudomonas aeruginosa infection in DG were all decreased. In the DG, the expressions of LC3-II and Beclin-1 were higher than in patients without ischemia than ischemic persons. Furthermore, the detection of LC3-II of macrophage was obviously lower in DG than CG.Conclusion: The drug resistance of PA and the detection rate of MARPA were higher for DFI patients. The expressions of autophagy are found in capillary endothelial cells, fibroblasts and inflammatory cells, but the level of autophagy especially the macrophage autophagy was lower in DFI patients. When DFI mergered with PA infection and ischemia, the level of autophagy in DFI decreased more obvious. As a result, to induce the cell autophagy may be a new way to treat DFI.