NADRB is a network aiming on bridging the knowledge gap in adaptive drug resistance and fitness properties of Gram-negative bacteria.
NADRB is an abbreviation for Network on Adaptive Drug Resistance of Bacteria. The network is financed by the Swedish Research Council.
Our aim
The network aims to mobilize efforts against the spread of life-threatening infections through exploration of the signalling pathways leading to adaptive drug resistance. By promoting research cooperation and information sharing among different actors, we envision a network that can stimulate the development of novel sustainable diagnostic and therapeutic strategies.
Background
In order to deal with the antibiotic resistance crisis, it is necessary to understand how bacterial pathogens acquire resistance as well as how they can become tolerant to antimicrobials. Generally, tolerance to antimicrobials can be intrinsic or adaptive. Intrinsic resistance to antibiotics is mediated through antibiotic resistance genes or alterations at genomic level whereas adaptive resistance is mediated by modification of bacterial life style through gene regulation. Communication through quorum sensing and biofilm formation are classical examples of bacterial adaptation leading the tolerance to environmental stresses and antibiotics.
Adaptive antibiotic resistance acts as an obstacle when treating biofilm-associated acute and chronic infections such as ventilator associated pneumonia caused by Pseudomonas aeruginosa, Acinetobacter baumannii, surgical wound infections, catheter-associated infections caused by Pseudomonas aeruginosa and Escherichia coli respectively, and gall stones infections caused by Salmonella Typhimurium.
Research questions being handled within the network
Do drug susceptibility patterns of bacteria relate to certain colony or cell morphotypes? The experimental setting is illustrated in a schematic diagram.
What kind of metabolic changes can drug susceptibility patterns of bacteria result in or be a result of?
What types of biofilms are associated with drug tolerance and how are they regulated?
Why are certain clonal types of bacteria prominent for persistent and extreme drug tolerance phenotypes?
What are the targets of c-di-GMP signalling that mediate drug tolerance and biofilm formation in Gram-negative bacteria?
Do the combinations of antibiotics and antibiofilm agents produce better antimicrobial effects in strong biofilm-producing bacterial isolates?
Schematic diagram tillustrating the flow of experimental work to explore adaptive drug tolerance mediated by colony phase switch in Acinetobacter baumannii.
ImageNADRB
Members of NADRB
Christian G. GiskeProfessor/Chief consultant physician Chairman of EUCAST , Karolinska Institutet and Karolinska University Hospital Stockholm