There are a few news articles that have been coming out (like this one) that draw attention to this recently published paper in ISME Journal, entitled “Iron availability shapes the evolution of bacteriocin resistance in Pseudomonas aeruginosa.” The big picture of the paper was to study how resistance evolves and to explore the effectiveness of antimicrobial peptides called bacteriocins. Haven’t heard of these abundant, naturally occurring proteins? They are considered narrow-spectrum antibiotics; you can think of antibiotics as bombs, and bacteriocins as drones with a programed target. Both are out to kill bacteria, one is just far more specific than the other. There are several different classes of bacteriocins that work in different ways, but the one they focused on in the above study was one that blocks a channel required for iron uptake. The researchers found that resistance to the pyocin S2 bacteriocin, which blocks iron uptake, was high in high iron conditions but low in low-iron conditions.
So what does this mean and what are the implications? First of all, it means that bacteriocins have the capacity to work as an antibiotic without bacteria gaining resistance to them under the right environmental conditions. Second of all, it means that there could, in theory, be a bacteriocin that targets specific superbugs that have evaded all of our antibiotics. And lastly, it means that if we know what bacteria spp. is causing an infection, we could treat it with a bacteriocin therapy rather than a broad-spectrum antibiotic in order to preserve our microbiomes.
Is this too good to be true? In my personal opinion, I say yes. Although there has been work done on bacteriocins for decades, there is still so so so much to learn before we could harness them for mass clinical use. We learned from this paper that environmental conditions are important, but that doesn’t get us very far either. The infections we want to treat are in the human body, which has more or less uniform and rigid environmental conditions across the world.
The abstract for the paper is below:
The evolution of bacterial resistance to conventional antimicrobials is a widely documented phenomenon with gravely important consequences for public health. However, bacteria also produce a vast repertoire of natural antimicrobials, presumably in order to kill competing species. Bacteriocins are a common class of protein-based antimicrobials that have been shown to have an important role in the ecology and evolution of bacterial communities. Relative to the evolution of antibiotic resistance, little is known about how novel resistance to these toxic compounds evolves. In this study, we present results illustrating that, although resistance is able to evolve, it remains critically dependent on the environmental context. Resistance to bacteriocins, in particular the pyocin S2, evolves readily when iron is present but less so when iron is limiting, because the receptor for this pyocin is also required for iron uptake during iron limitation. This suggests that although resistance to bacteriocins can easily evolve, environmental conditions will determine how and when resistance occurs.
Really interesting. Marine mammals sequester iron very, very early in inflammatory response. Maybe good model for more insight here?
Iron and hemes in the marine environment:, could it could be tested experimentally say with regards to Opportinistic growth and shifts in iron and ABR responses and enrich for strands of bacterocins with narrower spectres in relation to AKA superbugs ref NOVA BIOTICS in a safe manner at SHEDD ? Perhaps you have a case specific already ?
We really need a good backups Mcr-1 having in mind and http://pubs.rsc.org/en/Content/ArticleLanding/2014/MT/c4mt00031e#!divAbstract
BUT the again in terms of enriching for geongeneering purposes lurkes too perhaps not such good idea with regards to Marne phages /vira ?
Find me at http://www.sheddaquarium.org we can talk about study design. I think there are interesting possibilities.