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Targeting bacterial quorum sensing, rather than killing bacteria directly, offers a promising strategy against multidrug-resistant Pseudomonas aeruginosa. Screening FDA-approved drugs identified molecules, including Vorinostat, that inhibit the QS protein PqsE and reduce its enzymatic activity. Structural modifications may further disrupt bacterial communication and impair infection capability.
Traditional antibiotics kill bacteria or target their growth and replication. While this strategy has worked well for decades, it can lead to resistance—when mutated bacteria survive and continue to replicate, unbothered by the treatment.

In recent years, scientists have begun investigating another idea: What if we don't kill the bacteria but instead interfere with their communications and prevent them from launching a coordinated attack on the host? This approach might make it harder for bacteria to develop resistance. It's the foundation of a new approach, which targets quorum sensing (QS).

Image source: Springer Nature


Bacteria communicate with a chemical language, emitting molecules into their environment.
This is like radio communications among soldiers on a covert mission. Once they realize enough of their comrades have landed, they can start to connect and behave as a unit. Bacteria do something very similar.

Once a quorum has been reached, they begin to change their behaviour, moving from acting as individuals to acting as a group. They form colonies and secrete toxins. It's this coordinated attack that ultimately makes us sick.

By understanding and interfering with how bacteria talk to each other, researchers hope to develop a treatment for deadly bacterial diseases. 

Hannah A. Jones et al, Screening of FDA-Approved Small Molecules to Discover Inhibitors of the Pseudomonas aeruginosa Quorum-Sensing Enzyme, PqsE, Biochemistry (2026). DOI: 10.1021/acs.biochem.5c00475

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