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Liposomes Prevent in vitro Hemolysis Induced by Streptolysin O and Lysenin
Membranes
  • Marcelo Ayllon, Boise State University
  • Gamid Abatchev, Boise State University
  • Andrew Bogard, Boise State University
  • Rosey Whiting, Boise State University
  • Sarah E. Hobdey, Veteran Affairs Medical Center
  • Daniel Fologea, Boise State University
Document Type
Article
Publication Date
5-1-2021
Abstract

The need for alternatives to antibiotics in the fight against infectious diseases has inspired scientists to focus on antivirulence factors instead of the microorganisms themselves. In this respect, prior work indicates that tiny, enclosed bilayer lipid membranes (liposomes) have the potential to compete with cellular targets for toxin binding, hence preventing their biological attack and aiding with their clearance. The effectiveness of liposomes as decoy targets depends on their availability in the host and how rapidly they are cleared from the circulation. Although liposome PEGylation may improve their circulation time, little is known about how such a modification influences their interactions with antivirulence factors. To fill this gap in knowledge, we investigated regular and long-circulating liposomes for their ability to prevent in vitro red blood cell hemolysis induced by two potent lytic toxins, lysenin and streptolysin O. Our explorations indicate that both regular and long-circulating liposomes are capable of similarly preventing lysis induced by streptolysin O. In contrast, PEGylation reduced the effectiveness against lysenin-induced hemolysis and altered binding dynamics. These results suggest that toxin removal by long-circulating liposomes is feasible, yet dependent on the particular virulence factor under scrutiny.

Creative Commons License
Creative Commons Attribution 4.0 International
Citation Information
Marcelo Ayllon, Gamid Abatchev, Andrew Bogard, Rosey Whiting, et al.. "Liposomes Prevent in vitro Hemolysis Induced by Streptolysin O and Lysenin" Membranes (2021)
Available at: http://works.bepress.com/daniel_fologea/49/