BME seminar: Inflammasome and TRAP release contribute to medical device failure
This event is in the past.
Jean Gabriel de Souza, PhD, Wayne State University
Significant progress in implantable medical devices (IMD) including drug delivery systems and biomaterials has been realized over the past decades. Although these novel technologies improve the quality of life, poor IMD biocompatibility and underlying tissue damage caused by these systems could impede further advancement. In this presentation, we will cover current challenges to extending the lifespan of diabetes management devices, such as glucose sensors and insulin infusion sets. We will also discuss inflammasome and extracellular TRAP release in response to biomaterials. Inflammasomes and extracellular trap release are two potent mechanisms orchestrated mainly by macrophages and neutrophils in response to a spectrum of injuries. It is now stipulated that the initiation of these mechanism on biomaterials is a significant preconditioning event that influences device performance. Our data indicate that tissue responses at sites of IMD leads to cumulative cell/tissue toxicity, inflammation, and maladaptive wound healing. In vitro IMD and biomaterial toxicity studies include cell viability and netosis imaging assays using leukocytes from healthy and diabetic individuals. In vivo and in vitro studies conducted in mice and swine demonstrated device-induced cell death and neutrophil extracellular TRAPs (NET) formation. Chronic inflammation, fibrosis, blood vessel regression and granulation tissue are seen post 3-day device insertion. Future strategies designed to optimize device performance and longevity must mitigate pro-inflammatory factors arising from the drug preservatives, in the case of infusion sets, device materials and/or insertion site reactions to ensure tissue integrity.
Virtual and in-person event
Online: Zoom link
Join via: ID: 915 3281 4691 (Passcode: 835156)
In-person location: Biomedical Engineering, room 2220 (Map)