Study Presents New Insights on Genetic Dimensions and Resistance
Infections encountered in all the hospital-acquired bacterium Acinetobacter baumannii are exceptionally tough to deal with. The pathogen has developed several lines of defense against oxidative anxiety, such as a barrier-forming cell phone in addition to control systems that react to anti inflammatory stresses by bettering antibiotic resistance and virulence.
Now, a team of researchers at the Tufts University has demonstrated how A. baumannii builds this protective coating thereby allowing it to become more virulent as it continues to evade destruction from antibiotics. They found that the key is a network of molecules that turn specific genes on and off.
Using strains of this microbe which were genetically modified to activate or wipe from the BfmRS strain reaction, the research revealed that BfmRS empowers fatal sepsis in mice. They also analyzed these strains of Acinetobacter baumannii reacted to antibiotic exposure, discovering the BfmRS pressure response confers immunity to a vast array of drugs.
The study team also revealed that these consequences are linked to the genetic effect of BfmRS, demonstrating through RNA sequencing experiments it may reprogram gene expression through the A. baumannii genome.
Specifically, BfmRS controls many different genetic pathways involved with
construction and integrity of multiple elements of the cell phone in addition to cell division.Bottom line- the investigation showcases that BfmRS plays a key coordinating role in the intertwined ability of A. baumannii to put up resistance to antibiotics and boost virulence in response to them.
And this suggests that inhibition of BfmRS could serve as a potential strategy to combat A. baumannii.
“We revealed that a single two-protein system controls a global network of proteins that is critical for making A. baumannii a threat,” the authors further explain. “These proteins control broad drug resistance and the potential to cause opportunistic disease, and center on processes that build and maintain the cell envelope.”
