Good news! A welcome antidote to the deafening and long ongoing hysteria about antimicrobial resistance (AMR)!
Human ingenuity beats any bug (eventually)! It is an arms race, bugs can not win!
Now that we have also AI at our disposal, bugs have no chance anymore! We should actually feel sorry for bacteria! Caution: satire!
"... One such bacterium is Pseudomonas aeruginosa, which is naturally found in soil and water, but also hospitals, nursing homes and similar institutions for persons with weakened immune systems are home for strains of this bacterium. ...
Now, at team of researchers from Department of Biochemistry and Molecular Biology and Department of Clinical Microbiology, University of Southern Denmark, have discovered a weakness in P. aeruginosa with the potential to become the target for a new way to attack it. ..."
"The team discovered a mechanism, that reduces the formation of biofilm on the surface of P. Aeruginosa. The formation of sticky, slimy biofilm is a powerful tool used by bacteria to protect themselves against antibiotics – a trick also used by P. Aeruginosa.
- This biofilm can be so thick and gooey that antibiotic cannot penetrate the cell surface and reach its target inside the cell ...
- Maybe one day, we could pharmacologically stimulate this mechanism to reduce biofilm development on the surface of P. Aeruginosa. ...
Specifically, the researchers worked with three newly discovered genes in a lab-grown strain of P. aeruginosa. When they overexpressed these genes, they saw a strong reduction of biofilm. ..."
Specifically, the researchers worked with three newly discovered genes in a lab-grown strain of P. aeruginosa. When they overexpressed these genes, they saw a strong reduction of biofilm. ..."
From the abstract:
"Bacteriophages (hereafter “phages”) are ubiquitous predators of bacteria in the natural world, but interest is growing in their development into antibacterial therapy as complement or replacement for antibiotics. However, bacteria have evolved a huge variety of antiphage defense systems allowing them to resist phage lysis to a greater or lesser extent. In addition to dedicated phage defense systems, some aspects of the general stress response also impact phage susceptibility, but the details of this are not well known. In order to elucidate these factors in the opportunistic pathogen Pseudomonas aeruginosa, we used the laboratory-conditioned strain PAO1 as host for phage infection experiments as it is naturally poor in dedicated phage defense systems. Screening by transposon insertion sequencing indicated that the uncharacterized operon PA3040-PA3042 was potentially associated with resistance to lytic phages. However, we found that its primary role appeared to be in regulating biofilm formation, particularly in a clinical isolate of P. aeruginosa in which it also altered tobramycin resistance. Its expression was highly growth-phase dependent and responsive to phage infection and cell envelope stress. Our results suggest that this operon may be a cryptic but important locus for P. aeruginosa stress tolerance."
Researchers thwart resistant bacteria’s strategy (original news release) Bacteria are experts at evolving resistance to antibiotics. One resistance strategy is to cover their cell walls in sticky and gooey biofilm that antibiotics cannot penetrate. A new discovery could put a stop to this strategy.
Fig 2 Overexpression of the PA3040-PA3042 operon inhibits biofilm formation without affecting growth rate
Clare Kirkpatrick, the senior researcher
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