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

May 26, 2015 by Bob Yirka, report

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.

Explore further: Researchers find intestinal bacteria create phages for use as weapons

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

Related Stories

Research team recognizes predator-producing bacteria

December 11, 2012

Unique viruses called bacteriophages may play an important role in competition among bacterial strains, influencing the overall ecosystem of the human intestine, scientists at The University of Texas at Arlington and UT Southwestern ...

Antibiotic resistance is a gut reaction

December 16, 2014

Scientists from the Institute of Food Research and the University of East Anglia have discovered how certain gut bacteria can protect themselves and others in the gut from antibiotics.

Recommended for you

Droughts could hit aging power plants hard

March 26, 2019

Older power plants with once-through cooling systems generate about a third of all U.S. electricity, but their future generating capacity will be undercut by droughts and rising water temperatures linked to climate change. ...

Cellular microRNA detection with miRacles

March 26, 2019

MicroRNAs (miRNAs) are short noncoding regulatory RNAs that can repress gene expression post-transcriptionally and are therefore increasingly used as biomarkers of disease. Detecting miRNAs can be arduous and expensive as ...

What happened before the Big Bang?

March 26, 2019

A team of scientists has proposed a powerful new test for inflation, the theory that the universe dramatically expanded in size in a fleeting fraction of a second right after the Big Bang. Their goal is to give insight into ...

Probiotic bacteria evolve inside mice's GI tracts

March 26, 2019

Probiotics—which are living bacteria taken to promote digestive health—can evolve once inside the body and have the potential to become less effective and sometimes even harmful, according to a new study from Washington ...

Two new planets discovered using artificial intelligence

March 26, 2019

Astronomers at The University of Texas at Austin, in partnership with Google, have used artificial intelligence (AI) to uncover two more hidden planets in the Kepler space telescope archive. The technique shows promise for ...


Adjust slider to filter visible comments by rank

Display comments: newest first

1 / 5 (1) 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.
1 / 5 (2) 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."
1 / 5 (1) 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."

Please sign in to add a comment. Registration is free, and takes less than a minute. Read more

Click here to reset your password.
Sign in to get notified via email when new comments are made.