A warning about over-use of antibacterials
To patients and their families and friends.
There is concern about antibiotic immunity to about all drugs used to
combat them. This information from Steph Adams, science writer at
University of Illinois should chronicle the fact that the situation is
recognized and research is being done to solve the problem. We must thank
Professor Nair, postdoctoral researcher, Shi-Hui Dong, their colleagues and
of course Seph Adams for her permission to forward her article to you.
Respectfully,
Prostatitis Foundation
CHAMPAIGN, Ill. - Researchers at the University of Illinois have discovered
a mechanism that allows bacteria of the same species to communicate when
their survival is threatened. The study suggests that it may be possible to
slow dangerous infections by manipulating the messages these microbes send
to each other, allowing the body to defeat an infection without causing the
bacteria to develop resistance to the treatment.
The study, reported in the Proceedings of the National Academy of Sciences,
builds on work conducted by other researchers at Illinois, including
biochemist John Woodland Hastings, who died in 2014, and John Cronan, a professor and the
head of the department of microbiology
.
"Bacteria are intelligent little organisms. They can survive almost
anywhere and quickly adapt to new conditions," said U. of I. biochemistry
professor Satish Nair
, a co-author of the study
with postdoctoral researcher Shi-Hui Dong and other colleagues. Nair is the
director of the Center for Biophysics and Quantitative Biology
at Illinois.
When bacteria compete with other microbes for scarce resources, the more
successful group will produce a unique molecule = an antibiotic - to kill
off the other species. When population growth of one group of bacteria
outpaces availability of the nutrients it needs to survive, the group
produces another unique molecule that tells it to go into a dormant, but
more virulent, state and slow growth until more food is available, Nair
said.
"Ever since Alexander Fleming discovered penicillin in 1928, we have been
using antibiotic molecules developed by one microorganism to kill another
microorganism," Nair said. "Unfortunately, the bacteria have quickly
adapted to resist antibiotics, and in a short time, antibiotics will be
ineffective.
"On average, nearly every species of bacteria is resistant to at least one
antibiotic. Two years ago, researchers in Europe and Asia discovered a
so-called superbug that is resistant to all known antibiotics," Nair said.
"Bacteria can share adaptations very easily, and there are so many bacteria
with different adaptations to share, which is why they can develop
resistance so quickly."
"Broad-spectrum antibiotics and the overuse of antibiotics are problematic
because antibiotics kill off many types of bacteria, even good ones, and
the survivors figure out ways to adapt, sharing their strategies with other
bacteria," Dong said.
"No pharmaceutical company is going to invest in 10 years' worth of
research and development if a new antibiotic has a shelf-life of only two
years," Nair said. "It's not enough time to recover the costs of
production."
Nair and Dong's new study targets the language, or group signal, that
bacteria use to slow down growth rather than the antibiotic signal to kill.
The researchers say understanding how bacteria produce the dormancy-signal
molecule paves the way for developing molecules that can disrupt the
communication of specific bacteria, with little chance for drug resistance
to develop.
"We don't need to kill bacteria to treat disease and infection; we can
just slow them down and make them less potent," Nair said. "That way, there
is little chance for any resistance to develop."
Nair is an affiliate of the Carl R. Woese Institute for Genomic Biology
at Illinois. Research in the Nair lab is
funded by the National Institutes of Health.
*Editor's notes:*
To reach Satish Nair, call (217) 333-0641; email s-nair@life.illinois.edu.
The paper "Molecular basis for the substrate specificity of quorum signal
synthases" is available online
or from
the U. of I. School of Molecular and Cellular Biology.
DOI: 10.1073/pnas.1705400114
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