Indirect, Non-Thermal Atmospheric Plasma Promotes Bacterial Killing in vitro and Wound Disinfection in vivo Using Monogenic and Polygenic Models of Type 2 Diabetes (Without Adverse Metabolic Complications).

A novel atmospheric plasma device that uses indirect, non-thermal plasma generated from room air is being studied for its effects on wound disinfection in animal wounds of monogenic and polygenic murine models of type 2 diabetes. As a proof-of-concept report, the goal of this study was to demonstrate the efficacy and safety of the indirect non-thermal plasma (INTP) device in disinfecting polycarbonate filters established with Pseudomonas aeruginosa (PAO1) biofilms as well as wound disinfection in diabetic murine wounds. Dorsal excisional wounds in BALB/c, polygenic TALLYHO, and monogenic db/db mice established with PAO1 infection all demonstrated a 3-log colony-forming unit (CFU) reduction when subjected to a course of 20-min INTP treatments. Importantly, blood glucose and body weights in these animals were not significantly impacted by plasma treatment over the study period. Plasma safety was also analyzed via complete blood count and comprehensive metabolic panels, showing no deleterious systemic effects after 3 consecutive days of 20-min plasma applications. Therefore, the results obtained demonstrated the Pseudomonas aeruginosa isolates were highly sensitive to INTP in vitro, CFU reduction of infectious Pseudomonas in wounds of diabetic mice after INTP treatment is far superior to that of non-treated infected wounds, and the application of INTP shows no indication of toxic effects. Our results are consistent with indirect non-thermal atmospheric plasma as a promising adjunct to disinfecting wounds.

Sleep fragmentation delays wound healing in a mouse model of type 2 diabetes.

Study Objectives: This study tested the hypothesis that sleep fragmentation (SF) delays wound healing in obese B6.BKS(D)-Leprdb/J (db/db) mice with impaired leptin signaling and type 2 diabetes compared with wild-type C57BL/6J (B6) mice. Methods: Adult male mice (n = 34) were anesthetized and bilateral full-thickness excisional wounds were created on the back of each mouse. Half of the db/db and B6 mice were housed in SF cages equipped with a bar that moved across the cage floor every 2 min, 12 hr/day for 23 days. The other half of each group of mice was housed in the same room and did not experience SF. The dependent measures were number of days required to achieve wound closure, mRNA expression of four inflammatory mediators, blood glucose, insulin, and corticosterone. Results: SF in the db/db mice caused a significant delay in wound healing relative to db/db mice with no SF. Days to achieve 50 per cent wound healing were 13.3 ± 0.4 with SF compared with 10.3 ± 0.7 without SF. All B6 mice achieved 50 per cent wound healing within 6 days and complete healing after 16 days. SF caused a significant increase in wound levels of TNF-α mRNA only in the db/db mice and an increase in corticosterone only in the B6 mice. Conclusions: The delayed wound healing in obese, diabetic mice caused by SF is homologous to delayed wound healing in some patients with type 2 diabetes. The results support the interpretation that altered leptinergic signaling and inflammatory proteins contribute to delayed wound healing.