Scientists fool bacteria into programming own death
Every year, tens of thousands of women die in the EU from cervical cancer because the disease is not detected and treated at an early enough stage. A multidisciplinary European research effort plans to change that. Half of all the 60,000 new cases of cervical cancer diagnosed in Europe this year will prove to be
Full Post: European research effort pushes towards cervical cancer cure
Like firemen fighting fire with fire, researchers at the University of Illinois and the University of Massachusetts at Amherst have found a way to fool a bacteria’s evolutionary machinery into programming its own death.
“The basic idea is for an antimicrobial to target something in a bacteria that, in order to gain immunity, would require the bacteria to kill itself through a suicide mutation,” said Gerard Wong, a professor of materials science and engineering, of physics, and of bioengineering at the U. of I.
Wong is corresponding author of a paper accepted for publication in the Proceedings of the National Academy of Sciences . The paper is to be posted this week on the journal’s Web site.
The researchers show that a synthetic “hole punching” antimicrobial depends on the presence of phosphoethanolamine, a cone-shaped lipid found in high concentrations within Gram-negative bacterial membranes. Although PE lipids are commandeered to kill the bacteria, without the lipids the bacteria would die, also.
“It’s a Catch-22,” Wong said. “Some mutations bacteria can tolerate, and some mutations they cannot tolerate. In this case, the bacteria would have to go through a mutation that would kill it, in order to be immune to these antimicrobials.”
In their work, the researchers compared the survival of the bacterium Escherichia coli with that of a mutant strain of E. coli, which lacked PE lipids in its membrane. The fragile PE-deficient mutant strain out-survived the normal, healthy bacteria, when exposed to a “hole punching” synthetic antibiotic.
However, the opposite was true when both strains were exposed to tobramycin, a conventional metabolic antibiotic that targets the bacterial ribosomal machinery rather than the membrane.
The researchers first reported on compounds that functioned as molecular “hole punchers” last year in the Journal of the American Chemical Society. Their latest work further elucidates the “hole punching” mechanism.
“The antimicrobial re-organizes PE lipids into holes in the membrane,” said Wong, who also is a researcher at the university’s Beckman Institute. “The perforated membranes leak, and the bacteria die.”
Finding new ways to treat emerging pathogens that are more and more resistant to the best antibiotics will be increasingly important in the future, Wong said. “Now that we more fully understand how our molecular ‘hole punchers’ work, we can look for similar ways to make antimicrobials that bacteria cannot evolve immunity to.”
When bacterial infections cause us to get really sick, the only way to get better is to go to the doctor. With the help of antibiotics, we can start to recover quickly. One such antibiotic is Augmentin which belongs to the penicillin family of drugs. A bacterial infection is different to a viral infection, therefore the
Full Post: Antibiotic Augmentin
Scientists have identified the structure of a key component of the bacteria behind such diseases as whooping cough, peptic stomach ulcers and Legionnaires’ disease. The research, funded by the Wellcome Trust and the Biotechnology and Biological Sciences Research Council (BBSRC), sheds light on how antibiotic resistance genes spread from one bacterium to another. The research
Full Post: Discovery of novel ways to halt the spread of antibiotic resistance
As bacteria resistant to commonly used antibiotics continue to increase in number, scientists keep searching for new sources of drugs. In this week’s JBC, one potential new bactericide has been found in the tiny freshwater animal Hydra. The protein identified by Joachim Grötzinger, Thomas Bosch and colleagues at the University of Kiel, hydramacin-1, is unusual
Full Post: Discovery of potential new bactericide
In a paper available at the online site of the journal Biology of Reproduction, a team of UCLA researchers reports for the first time that vitamin D induces immune responses in placental tissues by stimulating production of the antimicrobial protein cathelicidin. The study involved exposing cultured human trophoblast cells to the active form of vitamin
Full Post: Vitamin D enhances placental innate immunity
Bacteria can occur almost anywhere on earth and exist under the most varying conditions. If these tiny, microscopic organisms are to survive in these environments, they need to be able to rapidly detect changes in their surroundings and react to them. Scientists at the Johannes Gutenberg University of Mainz are currently investigating how bacteria
Full Post: How the sensory organs of bacteria function