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posted by mrpg on Monday April 16 2018, @03:08PM   Printer-friendly
from the antibiotics++ dept.

A new class of antibiotics to combat drug resistance

Called odilorhabdins, or ODLs, the antibiotics are produced by symbiotic bacteria found in soil-dwelling nematode worms that colonize insects for food. The bacteria help to kill the insect and, importantly, secrete the antibiotic to keep competing bacteria away. Until now, these nematode-associated bacteria and the antibiotics they make have been largely understudied.

[...] UIC's Alexander Mankin and Yury Polikanov are corresponding authors on the study and led the research on the antibiotic's mechanism of action. They found that ODLs act on the ribosome — the molecular machine of individual cells that makes the proteins it needs to function — of bacterial cells. "Like many clinically useful antibiotics, ODLs work by targeting the ribosome," said Polikanov, assistant professor of biological sciences in the UIC College of Liberal Arts and Sciences, "but ODLs are unique because they bind to a place on the ribosome that has never been used by other known antibiotics."

Odilorhabdins, Antibacterial Agents that Cause Miscoding by Binding at a New Ribosomal Site (DOI: 10.1016/j.molcel.2018.03.001) (DX)

Meanwhile, an IBM research team has designed a polymer that can target at least five types of drug-resistant bacteria:

Earlier versions of synthetic polymers created problems because they essentially exploded the bacteria, releasing dangerous toxins into the bloodstream. While other scientists are researching different approaches to avoid resistance, most involve finding new molecules or proteins. IBM's synthetic molecule employs a completely different strategy.

It carries a negative electrical charge, so is drawn — like a magnet — to the positively charged surfaces of infectious cells. Then it binds to the cell, pierces the membrane, enters it and turns the inner liquid contents into solids. The new ninja polymer kills bacteria so quickly, they don't have time to mutate.

The eventual goal, said Hedrick, is to create an entirely new class of therapeutics that could treat a spectrum of infectious diseases with a single mechanism — without the onset of resistance.

Also at IBM.

A macromolecular approach to eradicate multidrug resistant bacterial infections while mitigating drug resistance onset (open, DOI: 10.1038/s41467-018-03325-6) (DX)


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  • (Score: 5, Interesting) by fyngyrz on Monday April 16 2018, @04:05PM (2 children)

    by fyngyrz (6567) on Monday April 16 2018, @04:05PM (#667675) Journal

    From TFS, emphasis mine:

    The eventual goal, said Hedrick, is to create an entirely new class of therapeutics that could treat a spectrum of infectious diseases with a single mechanism — without the onset of resistance

    Resistance doesn't (just) evolve from a lifeform that has received an insult; it also evolves because there are already versions of the lifeform that are resistant for whatever reason, and after the non-resistant ones are killed off, the resistant ones are the ones that remain to breed. These mutations may not have been common before, but can become common because they are no longer competing with non-resistant versions.

    Resistance, in general, can be a side effect of a mutation that has persisted for some other reason entirely.

    Having said that, this sounds like it's pretty powerful way to go about killing bacteria. Hope it works out.

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  • (Score: 2) by HiThere on Monday April 16 2018, @05:41PM (1 child)

    by HiThere (866) Subscriber Badge on Monday April 16 2018, @05:41PM (#667720) Journal

    The question is, does this anti-biotic also kill mammals? Other chordates?

    Since the bacteria kills it's host, it's clear that the anti-biotic it uses to protect it's food supply doesn't need to avoid killing anything but the bacteria itself.

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