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Access Type
WSU Access
Date of Award
January 2025
Degree Type
Thesis
Degree Name
M.S.
Department
Biomedical Engineering
First Advisor
Ulrike U. Klueh
Abstract
Advancements in transdermal glucose sensor systems have revolutionized diabetes care by enhancing glycemic control, which reduces the risk of subsequent microvascular and macrovascular complications. However, post-device implantation tissue reactions are inevitable. It is often speculated that the biocompatibility of the implanted material dictates the intensity and severity of the tissue reaction to these devices. Our data contradict this hypothesis as we demonstrated that the process of device insertion itself initiates an inflammatory response through neutrophil extracellular trap (NET) formation (NETosis) to an otherwise biocompatible sensor coating. Mouse studies demonstrated that acute inflammation primes the device surface for NETosis. Two weeks following sensor insertion in swine, regression in neovascularization in the sensor’s vicinity is apparent, while NETosis significantly decreased. Chronic inflammation, fibrosis, and granulation tissue were observed three days post-insertion in swine. These findings suggest that the trauma of sensor insertion initiates NETosis. Future strategies designed to optimize device performance and longevity must mitigate pro-inflammatory factors arising from the device insertion site’s tissue reactions.
Recommended Citation
Wood, Kenneth Adam, "Glucose Sensor Insertion Induces Inflammation Through Extracellular Trap Formation" (2025). Wayne State University Theses. 995.
https://digitalcommons.wayne.edu/oa_theses/995