Electro-microenvironment modulated inhibition of endogenous biofilms by piezo implants for ultrasound-localized intestinal perforation disinfection. (April 2023)

• Record Type: Journal Article
• Authors: Zhao, Xing; Wang, Li-Ya; Tang, Chun-Yan; Li, Kai; Huang, Yan-Hao; Duan, Yan-Ran; Zhang, Shu-Ting; Ke, Kai; Su, Bai-Hai; Yang, Wei
• Is Part Of: Biomaterials. Volume 295(2023)
• Publication Date: 2023-04
• Subjects: Antibacterial implants -- Piezoelectric nanofiber film -- Charge transfer -- Ultrasound treatment -- Intestinal disinfection; Biomedical materials -- Periodicals; Biocompatible Materials -- Periodicals; Biomatériaux -- Périodiques; 610.28
• DOI: 10.1016/j.biomaterials.2023.122055
• Languages: English
• ISSNs: 0142-9612

Abstract

Abstract: Endogenous bacterial infections from damaged gastrointestinal (GI) organs have high potential to cause systemic inflammatory responses and life-threatening sepsis. Current treatments, including systemic antibiotic administration and surgical suturing, are difficult in preventing bacterial translocation and further infection. Here, we report a wireless localized stimulator composed of a piezo implant with high piezoelectric output serving as an anti-infective therapy patch, which aims at modulating the electro-microenvironment of biofilm around GI wounds for effective inhibition of bacterial infection if combined with ultrasound (US) treatment from outside the body. The pulsed charges generated by the piezo implant in response to US stimulation transfer into bacterial biofilms, effectively destroying their macromolecular components ( e.g., membrane proteins), disrupting the electron transport chain of biofilms, and inhibiting bacterial proliferation, as proven by experimental studies and theoretical calculations. The piezo implant, in combination with US stimulation, also exhibits successful in vivo anti-infection efficacy in a rat cecal ligation and puncture (CLP) model. The proposed strategy, combining piezo implants with controllable US activation, creates a promising pathway for inhibiting endogenous bacterial infection caused by GI perforation.