Efficacy of silver-coated poly(ethylene terephthalate) to prevent bacterial attachment and subsequent infection was quantified in vitro, in both batch- and flowing-fluid experiments. Kinetic analysis of batch suspended cell cultures of Staphylococcus epidermidis (SE), at various growth-limiting nutrient concentrations, in the absence of any fabric, indicated a maximum culture growth rate constant micro(max) = 0.78 +/- 0.02 h(-1). Batch experiments for Control fabric samples indicated that SE cultures exhibited about the same suspended cell growth rate (0.72 +/- 0.02 h(-1)) as observed in batch suspended cultures without fabric. Suspended SE cultures in the presence of silver-coated fabric grew at a considerably lower rate, 0.15 +/- 0.01 h(-1), indicating the inhibitory effect of Ag(+2) ion released from the fabric. Growth rates of suspended SE cultures were 5-6 times higher in the fluid phase in contact with the Control fabric compared to cultures exposed to silver-coated fabric. Maximum suspended cell concentrations attained at time = 24 h were 1-2 orders of magnitude higher for Control fabrics vs. silver-coated fabric. In all batch colonization experiments, both live and dead SE bacterial cells accumulate on the surfaces of both silver-coated and Control fabrics. Adherent viable SE cells accumulated to 1-2 orders of magnitude more ( approximately 5 x 10(+8) cells/cm(2)) on Control fabric than SE cells on the silver-coated fabric ( approximately 1.1 x 10(+6) cells/cm(2)), respectively. Between 70-95% SE cells on the Control fabric were viable, while on the silver-coated fabric samples, at 24 h, viable cells were less than 10% of the adherent community (i.e., greater than 90% nonviable cells). In flow cell colonization experiments, SE cells accumulated on Control fabric to a maximum adherent cell concentration of 6 x 10(+7) - 8 x 10(+7) cells/cm(2) by 24 h with the proportion of viable cells remaining relatively constant at 76% throughout an experiment. Both noninvasive microscopic enumeration and destructive assays gave the same results for adherent cell numbers. Using silver-coated fabric, total cells numbers (live + dead) reached a level of approximately 1.1 x 10(+7) - 3.0 x 10(+7) cells/cm(2) after about 6 h and remained constant. However, while the proportion of viable cells initially on the surface was 63-75%, this fraction dropped continuously during each experiment to less than 6% viable cells at 24 h. Regardless of the criteria, the number of viable or nonviable cells attached to silver-coated fabric were significantly lower than on Control fabric.
Continuous Subcutaneous Insulin Infusion (CSII) is superior to conventional insulin therapy as it improves glycemic control thus reducing the probability of diabetic complications. Notwithstanding CSII's benefits, insulin dependent diabetic patients rarely achieve optimal glucose control. Moreover, CSII is only FDA approved for 3 days and often fails prematurely for reasons that have not been fully elucidated. We hypothesize that phenolic compounds, such as m‐cresol and phenol, which are present in all commercial insulin formulations are responsible for the tissue reaction occurring at the insulin infusion site. This hypothesis was examined with in vitro cell cultures and a mouse air‐pouch model to determine cellular and tissue reactions following infusions with saline, phenolic compounds, (i.e., commercial diluent), and insulin. We demonstrated that diluent and insulin were cytotoxic to cells in culture at sub‐clinical concentrations (e.g., >1:10 of commercial insulin). Air pouch studies demonstrated that infusion of either diluted insulin or diluent itself induced three to five‐fold level of recruited leukocytes as compared to saline. At both 3‐ and 7‐days post infusion, these were predominantly neutrophils and macrophages. We conclude that phenolic compounds in commercial insulin preparations are cell and tissue toxic, which contributes to the failure of effective insulin infusion therapy.
Little is known about the specific cells, mediators and mechanisms involved in the loss of glucose sensor function (GSF) in vivo. Since mast cells (MC) are known to be key effector cells in inflammation and wound healing, we hypothesized that MC and their products are major contributors to the skin inflammation and wound healing that controls GSF at sites of sensor implantation. To test this hypothesis we utilized a murine model of continuous glucose monitoring (CGM) in vivo in both normal C57BL/6 mice (mast cell sufficient), as well as mast cell deficient B6.Cg-Kit W-sh / HNihrJaeBsmJ (Sash) mice over a 28 day CGM period. As expected, both strains of mice displayed excellent CGM for the first 7 days post sensor implantation (PSI). CGM in the mast cell sufficient C57BL/6 mice was erratic over the remaining 21 days PSI. CGM in the mast cell deficient Sash mice displayed excellent sensor function for the entire 28 day of CGM. Histopathologic evaluation of implantation sites demonstrated that tissue reactions in Sash mice were dramatically less compared to the reactions in normal C57BL/6 mice. Additionally, mast cells were also seen to be consistently associated with the margins of sensor tissue reactions in normal C57BL/6 mice. Finally, direct injection of bone marrow derived mast cells at sites of sensor implantation induced an acute and dramatic loss of sensor function in both C57BL/6 and Sash mice. These results demonstrate the key role of mast cells in controlling glucose sensor function in vivo.
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