2015 journal article

Membrane-Permeabilizing Activity of Reverse-Amide 2-Aminoimidazole Antibiofilm Agents Against Acinetobacter baumannii

CURRENT DRUG DELIVERY, 12(2), 223–230.

By: S. Stowe*, R. Thompson*, L. Peng*, Z. Su*, M. Blackledge*, G. Draughn, W. Coe, E. Johannes* ...

author keywords: 2-aminoimidazole; Acinetobacter baumannii; biofilm; membrane permeabilization; reverse amide; SEM
MeSH headings : Acinetobacter baumannii / drug effects; Amides / chemistry; Anti-Bacterial Agents / chemistry; Anti-Bacterial Agents / pharmacology; Biofilms / drug effects; Cell Membrane Permeability / drug effects; Cells, Cultured; Cross Infection; Imidazoles / chemistry; Imidazoles / pharmacology; Microbial Sensitivity Tests
TL;DR: A model is proposed that describes how the structure of RA-2AI allows it to insert itself into and disrupt the fluidity of the membrane, creating an opportunity for increased molecular permeability. (via Semantic Scholar)
UN Sustainable Development Goal Categories
Source: Web Of Science
Added: August 6, 2018

Acinetobacter baumannii has quickly become one of the most insidious and prevalent nosocomial infections. Recently, the reverse-amide class of 2-aminoimidazole compounds (RA-2AI) was found both to prevent A. baumannii biofilm formation and also to disperse preexisting formations, putatively through interactions with cytosolic response regulators. Here we focus on how this class of antibiofilm agent traverses cellular membranes. Following the discovery of dosage-dependent growth rate changes, the cellular effects of RA-2AI were investigated using a combination of molecular assays and microscopic techniques. It was found that RA-2AI exposure has measureable effects on the bacterial membranes, resulting in a period of increased permeability and visible structural aberrations. Based on these results, we propose a model that describes how the structure of RA-2AI allows it to insert itself into and disrupt the fluidity of the membrane, creating an opportunity for increased molecular permeability.