IIT Roorkee Researchers Discover Superbug Defense Mechanism to Enhance Treatment Approaches
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Synopsis
A team from IIT Roorkee has unveiled a key defense mechanism in the superbug Acinetobacter baumannii. This discovery could lead to improved treatments for drug-resistant infections, revealing how the pathogen regulates its attack systems.
Key Takeaways
- Discovery of a regulatory mechanism in a superbug.
- Understanding T6SS and its role in antibiotic resistance.
- Influence of manganese on the superbug's defenses.
- Potential for targeted therapy through AbsR28.
- Implications for precision medicine and drug development.
Roorkee, Feb 10 (NationPress) Researchers at the Indian Institute of Technology (IIT) Roorkee have identified a significant regulatory mechanism in Acinetobacter baumannii -- a notorious drug-resistant superbug linked to severe infections.
Their findings, published in the journal mBio, illuminate how this pathogen manages its offensive and defensive strategies, which could inform the development of innovative treatment options.
Acinetobacter baumannii represents a substantial risk in medical environments due to its ability to resist numerous antibiotics. It is responsible for critical hospital-acquired infections such as pneumonia, bloodstream infections, and urinary tract infections.
To combat rival microbes, this superbug utilizes the Type 6 Secretion System (T6SS) -- a bacterial “weapon”. However, the exact mechanism that allows it to sustain antibiotic resistance has remained elusive until now.
The research team, headed by Prof. Ranjana Pathania, found that A. baumannii can toggle T6SS on or off depending on its surroundings. They discovered that a small RNA molecule -- AbsR28 -- is critical in this regulation, which is influenced by manganese concentrations.
When manganese levels are elevated, AbsR28 attaches to a vital gene (tssM) necessary for T6SS functionality. This process leads to the gene's degradation and inhibits T6SS activation, according to the researchers.
Higher manganese levels also allow A. baumannii to preserve plasmid pAB3, which harbors many antibiotic-resistance genes.
“We discovered that when A. baumannii activates T6SS, it becomes increasingly vulnerable to antibiotics and oxidative stress. Thus, the bacteria must meticulously regulate this system to endure varying conditions,” explained Prof. Pathania.
“Our research provides insight into how this pathogen adjusts during infections, allowing it to avoid both antibiotics and the immune response,” she added.
The results indicated that targeting AbsR28 could disrupt the superbug's regulatory mechanisms, increasing its sensitivity to antibiotics without directly impacting resistance genes. This breakthrough also paves the way for precision medicine and new drug development aimed at tackling multidrug-resistant infections.
