Pheromones produced by gut bacteria found to kill resistant variants of its own kind

This photomicrograph reveals cocci-shaped Enterococcus sp. bacteria taken from a pneumonia patient. Enterococcus sp. is a common, gram-positive bacterium that can normally be found in the bowel and female genital tract. These bacteria can be spread by fecal-oral transmission, contact with infected body fluids or contact with contaminated surfaces. Credit: CDC/public domain

(—A team of researchers with members from Harvard Medical School and the University of Kansas has found that pheromones produced by one type of non-resistant bacteria can kill other bacteria that have grown resistant to agents meant to kill them. In their paper published in Proceedings of the National Academy of Sciences, the team describes how they discovered such occurrences while investigating mobile elements and metabolic pathways of resistant bacteria.

Over the past decade it has become clear to scientists that are winning the war against them by us humans—as we develop new agents to kill them, they develop new ways to avoid being killed by them, some of which include mobile elements that encode virulence and antibiotic resistance traits and new . In this new effort, the researchers were investigating the ways that bacteria evolve to cause themselves to become resistant to new antibiotics, when they discovered that one strain of human gut bacteria, Enterococcus, produces a pheromone that is lethal to other strains of the same type of bacteria.

More specifically, they found that a non-resistant strain of Enterococcus (which is native to the human gut) produced a pheromone called cOB1—when drug resistant E. faecalis V583 bacteria were exposed to that pheromone, they were killed. This finding is important because it shows that native healthy non- might prove useful in fighting resistant bacterial infections. But more immediately, it shows that it might be possible to use friendly strains of Enterococcus right away to stop resistant bacterial infections in the gut. E. faecalis V583 are a leading cause of hospital acquired infections—they tend to move in to the gut when patients are given antibiotics to ward off infections after surgery and incidentally kill off all or most of the gut biota. This new work suggests such a problem might be averted by simply feeding surgical patients a liquid chock full of , possibly taken from their own gut, prior to surgery.

The team notes that normally E. faecalis V583 are unable to compete with the healthy strains of Enterococcus, because they have a number of mobile genetic elements in their genome that likely hinder their ability to compete with native bacteria—in the absence of antibiotics. It is only when antibiotics are introduced that E. faecalis V583 gain an advantage and multiply rapidly, causing a gut infection.

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More information: Pheromone killing of multidrug-resistant Enterococcus faecalis V583 by native commensal strains, PNAS,

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Citation: Pheromones produced by gut bacteria found to kill resistant variants of its own kind (2015, May 26) retrieved 19 October 2019 from
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May 27, 2015
The ability of pheromones to control the growth of variant strains involves self vs nonself recognition and attests to their ability to control virus-driven cell type proliferation.

It exemplifies everything known to serious scientists about the biophysically constrained chemistry of nutrient-dependent RNA-mediated protein folding.

Thermodynamic cycles of protein biosynthesis and degradation link viral microRNAs to entropic elasticity, and also link the anti-entropic epigenetic effects of nutrient-dependent microRNAs to RNA-mediated amino acid substitutions that stabilize the organized genomes of species from microbes to man. The amino acid substitutions are fixed in the context of pheromone-controlled reproduction.

The nutrient-dependent pheromone-controlled physiology of reproduction links feedback loops to chromatin loops and the organization of all genomes. The more organized genomes signal their ability to suppress viral damage to DNA via pheromones.

May 27, 2015
Placing the innate ability of the bacterial immune system to protect us and them against viruses into the context of evolution and antibiotic resistance is a way to keep promoting the ridiculous pseudoscientific nonsense of the evolution industry.

Serious scientists have linked protection against viral microRNAs that perturb protein folding from the nutrient-dependent pheromone-controlled life cycles of bioluminescent bacteria in squid to the nutrient-dependent pheromone-controlled reproduction of the squid.

"Bonnie Bassler discovered that bacteria "talk" to each other, using a chemical language that lets them coordinate defense and mount attacks. The find has stunning implications for medicine, industry — and our understanding of ourselves.

Bonnie Bassler studies how bacteria can communicate with one another, through chemical signals, to act as a unit. Her work could pave the way for new, more potent medicine."

May 27, 2015
bacteria evolve to cause themselves to become resistant to new antibiotics

If so, we would have created ourselves from bacteria and "evolved" our ability to resist the damage caused by the virus-driven proliferation of undifferentiated cell types found in cancers.

Instead, the ability of species from microbes to humans to adapt to ecological variation arises in the context of the nutrient-dependent pheromone-controlled physiology of reproduction.

That means ecological adaptations are biophysically constrained by the nutrient-dependent chemistry of RNA-mediated protein folding. RNA-mediated amino acid substitutions are the biophysical constraints that prevent pathology.

For comparison, see this claim: "...genomic conservation and constraint-breaking mutation is the ultimate source of all biological innovations and the enormous amount of biodiversity in this world."

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