COLUMBUS, Ohio Scientists have identified the role of two proteins that contribute to disease-causing bacteria cells versatility in resisting certain classes of antibiotics.
The finding is a step toward development of drug therapies that could target bacterial resistance at its cellular source. Before researchers can design such drugs, they must understand all of the activities at play in the conflict between bacteria and the agents that kill them.
This finding by Ohio State University microbiologists extends the understanding of how bacteria cells resist antibiotics through the activities of two genetically distinct forms of what are called MprFs, or multiple peptide resistance factors. The proteins they studied are MprF1 and MprF2.
These proteins were found to be key to the mechanism allowing bacteria cells to change the electrical charge of their membrane, which is how the cells develop their resistance to certain antimicrobial agents and, more generally, how they adapt their membrane to new environmental conditions, such as those provided by their host organism.
Both of these proteins are potentially very good drug targets because in theory, if you can target them and inhibit their action, you can make bacteria strains more susceptible to existing antibiotics, said Michael Ibba, associate professor of microbiology at Ohio State and a coauthor of the study.
The findings are described online in this weeks issue of Proceedings of the National Academy of Sciences.
Scientists have already observed that the cell membranes of many disease-causing bacteria develop resistance by changing their electrical charge from negative to positive. Many antibiotics work because they carry a positive charge that attracts them to negatively charged bacteria cells. The opposite charges allow antibiotics to penetrate and kill bacteria. But by changing their naturally occurring negative charge to positive, some bacteria cell
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Ohio State University