Topic: Biology

Australian researchers developed an antibody that targets a unique sugar found only on bacterial cells. This breakthrough could lead to new treatments for drug-resistant infections.

Researchers in Australia have made a significant discovery that could help combat deadly bacteria that no longer respond to antibiotics. They engineered antibodies that lock onto a specific sugar found only on bacterial cells. This approach could support the development of new immunotherapies for multidrug resistant infections acquired in hospitals.

The study, published in Nature Chemical Biology, shows that an antibody created in the laboratory was able to eliminate a normally fatal bacterial infection in mice. The antibody works by binding to this distinctive bacterial sugar and alerting the immune system to destroy the invading pathogen.

This project was co-led by Professor Richard Payne of the University of Sydney, working with Professor Ethan Goddard Borger at WEHI and Associate Professor Nichollas Scott from the University of Melbourne and the Peter Doherty Institute for Infection and Immunity. Professor Payne is also set to lead the newly announced Australian Research Council Centre of Excellence for Advanced Peptide and Protein Engineering.

The team targeted a sugar molecule called pseudaminic acid, which is made only by bacteria. This unique target offers a highly specific way to develop immunotherapies that avoid harming healthy cells.

Designing a broad-acting antibody required the researchers to first synthesize the bacterial sugar and decorated peptides entirely from scratch. This work allowed them to determine the molecule's exact three-dimensional structure and how it appears on bacterial surfaces.

Using this detailed information, the team created what they describe as a 'pan-specific' antibody that can recognize the same sugar across many different bacterial species and strains. In mouse infection studies, the antibody successfully cleared multidrug-resistant Acinetobacter baumannii, a bacterium that is a well-known cause of hospital-acquired pneumonia and bloodstream infections.

Passive immunotherapy involves giving patients ready-made antibodies to quickly control an infection, rather than waiting for the body's adaptive immune system to respond. This approach can be used both to treat active infections and prevent them. In hospital settings, it could be used to protect vulnerable patients in intensive care units who are at high risk from drug-resistant bacteria.

The antibodies also offer an important new way to study how bacteria cause disease. 'These sugars are central to bacterial virulence, but they've been very hard to study,' Associate Professor Scott noted. 'Having antibodies that can selectively recognize them lets us map where they appear and how they contribute to infection.'

This breakthrough has the potential to lead to new life-saving treatments for patients with multidrug-resistant infections.

Why It Matters

This discovery could help save lives by providing a new way to combat deadly bacteria that no longer respond to antibiotics. It's especially important in India, where hospital-acquired infections are a significant concern.

Key Facts

• Australian researchers developed an antibody that targets a unique sugar found only on bacterial cells.
• The antibody was able to eliminate a normally fatal bacterial infection in mice.
• The team used synthetic chemistry to build the bacterial sugar and decorated peptides from scratch.
• The 'pan-specific' antibody can recognize the same sugar across many different bacterial species and strains.
• Passive immunotherapy could be used to protect vulnerable patients in intensive care units who are at high risk from drug-resistant bacteria.

Key Terms

Pseudaminic acid

A unique sugar molecule found only on bacterial cells

Implications

This discovery could help save lives by providing a new way to combat deadly bacteria that no longer respond to antibiotics. It's especially important in India, where hospital-acquired infections are a significant concern.