New proteins from cold: antibiofilm activity of Cold-Azurin and PsyOmp38 against Enterococcus sp. and Klebsiella pneumoniae

The development of antimicrobial resistance is a very complex mechanism, sometimes due to phenotypic variations of the microbial community rather than to the appearance of genetic mutations. A phenotypic variant is certainly the ability of bacteria to form biofilms, in which they are incorporated into a matrix of self-produced extracellular polymeric substances. Biofilm formation is a physiological condition that provides bacteria with protection from the action of the immune system and antimicrobial agents. In the present study, attention was given to Enterococcus spp and Klebsiella pneumoniae , belonging to ESKAPE pathogens, commonly causing healthcare-associated infections, also for their ability to form biofilms. K. pneumoniae and Enterococcus spp are often together associated with a high risk of urinary tract infections due to biofilm-related complications in indwelling devices, commonly used in urological surgery. Currently, research is focusing on the development of new therapeutic strategies aimed at targeting bacterial virulence factors, such as biofilm, to reduce the increasing development of multidrug-resistant pathogens. In this context, microorganisms capable of thriving in extreme environments are of particular interest. In extreme environments, Antarctic marine bacteria have developed survival strategies aimed at reducing the presence of competing microorganisms. In the present research, the activity of Psy Omp38 and Cold-Azurin was evaluated on a collection of clinical Enterococcus spp. and K. pneumoniae strains. Both proteins are able to impair, with different capabilities, biofilm formation of almost all bacterial tested strains.